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PHYSIOLOGICAL PSYCHOLOGY III SEMESTER Complementary Course for B.Sc. Counselling Psychology (CUCBCSS - 2014 Admission onwards) UNIVERSITY OF CALICUT SCHOOL OF DISTANCE EDUCATION STUDY MATERIAL Core Course B.Sc. COUNSELLING PSYCHOLOGY III Semester UNIVERSITY OF CALICUT physiological psychology SCHOOL OF DISTANCE EDUCATION Calicut university P.O, Malappuram Kerala, India 673 635. School of Distance Education UNIVERSITY OF CALICUT SCHOOL OF DISTANCE EDUCATION STUDY MATERIAL PHYSIOLOGICAL PSYCHOLOGY III Semester Complementary Course B.Sc. Counselling Psychology Prepared by : Sri. Mohammed Junaid. A, Research scholar, Dept. of Psychology, Calicut University. Scrutinized by: Dr. Baby Shari P A, Associate Professor, Dept. of Psychology, Calicut University. Layout & Settings: Computer Section, SDE © Reserved 2 Physiological Psychology School of Distance Education PAGES CONTENT I 05-29 Module - II 30-40 Module - 3 Physiological Psychology School of Distance Education 4 Physiological Psychology School of Distance Education MODULE 1 SENSORY PROCESSES OTHER THAN VISION THE SENSE OF HEARING Structures of the outer, middle, and inner ear are involved in the sense of hearing. The inner ear also contains structures that provide a sense of balance, or equilibrium. The development of the ear begins during the fourth week and is complete by week 32. The ear contains receptors that convert sound waves into nerve impulses and receptors that respond to movements of the head. Impulses from both receptor types are transmitted through the vestibule-cochlear nerve to the brain for interpretation. Outer Ear The outer ear consists of the auricle, or pinna, and the external acoustic canal. The external acoustic canal is the fleshy tube that is fitted into the bony tube called the external acoustic meatus. The auricle is the visible fleshy appendage attached to the side of the head. It consists of a cartilaginous framework of elastic connective tissue covered with skin. The rim of the auricle is the helix, and the inferior fleshy portion is the earlobe. The earlobe is the only portion of the auricle that is not supported with cartilage. The auricle has a ligamentous attachment to the skull and poorly developed auricular muscles that insert within it anteriorly, superiorly, and posteriorly. The blood supply to the auricle is from the posterior auricular and occipital arteries, which branch from the external carotid and superficial temporal arteries, respectively. The structure of the auricle directs sound waves into the external acoustic canal. The external acoustic canal is a slightly S-shaped tube, about 2.5 cm long,that extends slightly upward from the auricle to the tympanic membrane. The skin that lines the canal contains fine hairs and sebaceous glands near the entrance. Deep within the canal, the skin contains specialized wax secreting glands, called ceruminous glands. The cerumen (earwax) secreted from these glands keeps the tympanic membrane soft and waterproof. The cerumen and hairs also help to prevent small foreign objects from reaching the tympanic membrane. The bitter cerumen is probably an insect repellent as well. The tympanic membrane (“eardrum”) is a thin, double-layered, epithelial partition, approximately 1 cm in diameter, between the external acoustic canal and the middle ear. It is composed of an outer concave layer of stratified squamous epithelium and an inner convex layer of low columnar epithelium. Between the epithelial layers is a layer of connective tissue. The tympanic membrane is extremely sensitive to pain and is innervated by the auriculotemporal nerve (a branch of the mandibular nerve of the trigeminal nerve) and the auricular nerve (a branch of the vagus nerve). Small sensory branches from the facial nerve and the glosopharyngeal nerve also innervate the tympanic membrane. 5 Physiological Psychology School of Distance Education Middle Ear The laterally compressed middle ear is an air-filled chamber called the tympanic cavity in the petrous part of the temporal bone. The tympanic membrane separates the middle ear from the external acoustic canal of the outer ear. A bony partition containing the vestibular window (oval window) and the cochlear window (round window) separates the middle ear from the inner ear. There are two openings into the tympanic cavity. The epitympanic recess in the posterior wall connects the tympanic cavity to the mastoidal air cells within the mastoid process of the temporal bone. The auditory (eustachian) tube connects the tympanic cavity anteriorly with the nasopharynx and equalizes air pressure on both sides of the tympanic membrane. Three auditory ossicles extend across the tympanic cavity from the tympanic membrane to the vestibular window. These tiny bones (the smallest in the body), from outer to inner, are the malleus (hammer), incus (anvil), and stapes (stirrup). The auditory ossicles are attached to the wall of the tympanic cavity by ligaments. Vibrations of the tympanic membrane cause the auditory ossicles to move and transmit sound waves across the tympanic cavity to the vestibular window. Vibration of the vestibular window moves a fluid within the inner ear and stimulates the receptors of hearing. As the auditory ossicles transmit vibrations from the tympanic membrane, they act as a lever system to amplify sound waves. In addition, the sound waves are intensified as they are transmitted from the relatively large surface of the tympanic membrane to the smaller surface area of the vestibular window. The combined effect increases sound amplification about 20 times. Two small skeletal muscles, the tensor tympani muscle and the stapedius muscle, attach to the malleus and stapes, respectively, and contract reflexively to protect the inner ear against loud noises. When contracted, the tensor tympani muscle pulls the malleus inward, and the stapedius muscle pulls the stapes outward. This combined action reduces the force of vibration of the auditory ossicles. Inner Ear The entire structure of the inner ear is referred to as the labyrinth. The labyrinth consists of an outer shell of dense bone called the bony labyrinth that surrounds and protects a membranous labyrinth. The space between the bony labyrinth and the membranous labyrinth is filled with a fluid called perilymph, which is secreted by cells lining the bony canals. Within the tubular chambers of the membranous labyrinth is yet another fluid called endolymph. These two fluids provide a liquid-conducting medium 6 Physiological Psychology School of Distance Education for the vibrations involved in hearing and the maintenance of equilibrium. The bony labyrinth is structurally and functionally divided into three areas: the vestibule, semicircular canals, and cochlea. The functional organs for hearing and equilibrium are located in these areas. Vestibule The vestibule is the central portion of the bony labyrinth. It contains the vestibular (oval) window, into which the stapes fits, and the cochlear (round) window on the opposite end. The membranous labyrinth within the vestibule consists of two connected sacs called the utricle and the saccule. The utricle is larger than the saccule and lies in the upper back portion of the vestibule. Both the utricle and saccule contain receptors that are sensitive to gravity and linear movement (acceleration) of the head. Semicircular Canals Posterior to the vestibule are the three bony semicircular canals, positioned at nearly right angles to each other. The thinner semicircular ducts form the membranous labyrinth within the semicircular canals. Each of the three semicircular ducts has a membranous ampulla at one end and connects with the upper back part of the utricle. Receptors within the semicircular ducts are sensitive to angular acceleration and deceleration of the head, as in rotational movement. Cochlea The snail-shaped cochlea is coiled two and a half times around a central core of bone. There are three chambers in the cochlea. The upper chamber, the scala vestibuli, begins at the vestibular window and extends to the apex (end) of the coiled cochlea. The lower chamber, the scala tympani, begins at the apex and terminates at the cochlear window. Both the scala vestibuli and the scala tympani are filled with perilymph. They are completely separated, except at the narrow apex of the cochlea, called the helicotrema where they are continuous. Between the scala vestibuli and the scala tympani is the cochlear duct, the triangular middle chamber of the cochlea. The roof of the cochlear duct is called the vestibular membrane, and the floor is called the basilar membrane. The cochlear duct, which is filled with endolymph, ends at the helicotrema. Within the cochlear duct is a specialized structure called the spiral organ (organ of Corti). The sound receptors that transform mechanical vibrations into nerve impulses are located along the basilar membrane of this structure, making it the functional unit of 7 Physiological Psychology School of Distance Education hearing. The epithelium of the spiral organ consists of supporting cells and hair cells. The bases of the hair cells are anchored in the basilar membrane, and their tips are embedded in the tectorial membrane, which forms a gelatinous canopy over them. Sound Waves and Neural Pathways for Hearing Sound Waves Sound waves travel in all directions from their source, like ripples in a pond after a stone is dropped. These waves of energy are characterized by their frequency and their intensity. The frequency, or number of waves that pass a given point in a given time, is measured in hertz (Hz). The pitch of a sound is directly related to its frequency—the higher the frequency of a sound, the higher its pitch. For example, striking the high C on a piano produces a high frequency of sound that has a high pitch. The intensity, or loudness of a sound, is directly related to the amplitude of the sound waves. Sound intensity is measured in units known as decibels (dB). A sound that is barely audible—at the threshold of hearing—has an intensity of zero decibels. Every 10 decibels indicates a tenfold increase in sound intensity: a sound is 10 times higher than threshold at 10 dB, 100 times higher at 20 dB, a million times higher at 60 dB, and 10 billion times higher at 100 dB. The healthy human ear can detect very small differences in sound intensity— from 0.1 to 0.5 dB. Sound waves funneled through the external acoustic canal produce extremely small vibrations of the tympanic membrane. Movements of the tympanum during ordinary speech (with an average intensity of 60 dB) are estimated to be equal to the diameter of a molecule of hydrogen. Sound waves passing through the solid medium of the auditory ossicles are amplified about 20 times as they reach the footplate of the stapes, which is seated within the vestibular window. As the vestibular window is displaced, pressure waves pass through the fluid medium of the scala vestibuli and pass around the helicotrema to the scala tympani. Movements of perilymph within the scala tympani, in turn, displace the cochlear window into the tympanic cavity. When the sound frequency (pitch) is sufficiently low, there is adequate time for the pressure waves of perilymph within the scala vestibuli to travel around the helicotrema to the scala tympani. As the sound frequency increases, however, these pressure waves do not have time to travel all the way to the apex of the cochlea. Instead, they are transmitted through the vestibular membrane, which separates the scala vestibuli from the cochlear duct, and through the basilar membrane, which separates the cochlear 8 Physiological Psychology School of Distance Education duct from the scala tympani, to the perilymph of the scala tympani. The distance that these pressure waves travel, therefore, decreases as the sound frequency increases. Neural Pathways for Hearing Cochlear sensory neurons in the vestibulocochlear nerve synapse with neurons in the medulla oblongata, which project to the inferior colliculi of the midbrain. Neurons in this area in turn project to the thalamus, which sends axons to the auditory cortex of the temporal lobe, where the auditory sensations (nerve impulses) are perceived as sound. AUDITORY LOCALIZATION The process of recognizing where a sound is coming from is analogous to recognizing depth or distance in vision. Both processes involve spatial aspects of sensory input. Many features contribute to auditory localization of which the following are most important: Having two ears In the same way that having two eyes allows for greater visual abilities through stereoscopic vision, so having two ears affords a greater skill in hearing. The use of two ears is called binaural detection. Without two ears, our ability to locate a sound source is diminished, although, as we shall see, not completely eradicated. Phase difference and sonic shadow When sound comes from one side or the other, two cues are available to help locate its source. The first cue comes from the fact that the sound will reach one ear prior to the other. This creates an arrival time difference (also known as a latency difference), which can be detected by neurons in the superior olive. Cells here are tuned to particular arrival time differences and can detect differences in arrival time at the two ears that are as small as a fraction of a millisecond. Differences in arrival time are adequate to locate a sound source if the sound is a simple and discrete one (for example, a click), but a variation of this is needed to explain our ability to locate more complex or continuous sounds. Phase difference Phase difference refers to the fact that different portions (phases) of the sound wave arrive at each ear at any one time. That is, while one ear is stimulated by a high pressure part of the sound wave, the other might be stimulated by a lower pressure part. These phase differences have the following consequence. Sound waves cause the eardrum to be pushed in and pulled out (i.e. to vibrate). Phase differences will mean that whilst, 9 Physiological Psychology School of Distance Education say, the right eardrum is pushed in, the left eardrum might simultaneously be pulled out. If the eardrum positions were exactly opposite, then the phase difference would be 180˚. Given that the phase difference for sounds directly in the midline will be zero and the maximal phase difference is 180˚, the combination of phase difference and sound frequency will give an indication of the sound’s location. This information is more useful for low frequency sounds than for high frequency sounds because of the wavelength and the distance separating the ears. Neurons of the medial superior olive are able to use this phase difference as an aid to locating the source of the sound. A second cue to location comes from sound intensity differences that arise from what is called the sonic shadow. This method of detection is particularly useful for high frequency sounds when the phase differences become too small to detect as the wavelengths of the sound become shorter. Information that comes from one side of the head will be more intense in the nearer ear and less intense in the further ear. The head is in the way of the further ear and absorbs high frequency sounds. Cells in the lateral superior olive and the auditory cortex can detect these intensity differences. These two mechanisms are complementary, providing a comprehensive system for the localization of sounds. Low frequency sounds produce phase differences but do not produce great differences in intensity at the two ears. Higher-frequency sounds produce poor phase differences but create a strong sonic shadow. The combination of both mechanisms allows for the detection of the location of sound across the whole frequency range and is known as the duplex theory. Monaural cues People who are deaf in one ear are not completely unable to localize sound. Monaural cues to the location of sound come from the pinnae of the outer ear. The pinnae dampen and filter the sound that enters the ear canal (known as spectral filtering). The modulations that occur will depend in part on the direction that the sound is coming from. Our ability to detect these differences gives us a localization cue. We need to appreciate here that our ability to recognize these changes alters as our head and ears grow from childhood into adulthood. Differentiating ‘in front’ from ‘behind Two sounds that are located an equal distance from your ears in the midline, where one is in front and one is behind, will be difficult to distinguish. There will be no difference of phase or latency, and the intensities of the sounds at the two ears will be identical. The knowledge of whether the sound is coming from in front or from behind relies on the 10 Physiological Psychology School of Distance Education pinnae of the outer ear. The differences in reflection of sound by the folds of the pinnae will differ for the two sound sources. Interestingly, sound location is best in the horizontal plane and much poorer for the near–far, in front–behind, and up–down directions. THEORIES OF HEARING Theories of hearing account for how sound waves are physiologically translated into the perceptions of pitch, loudness, and timbre. To date, most of the theorizing about hearing has focused on the perception of pitch, which is reasonably well understood. Researchers’ understanding of loudness and timbre perception is primitive by comparison. Hence, we’ll limit our coverage to theories of pitch perception. Two theories have dominated the debate on pitch perception: place theory and frequency theory. For better understatnding of these theories, imagine the spiraled cochlea unraveled, so that the basilar membrane becomes a long, thin sheet, lined with about 25,000 individual hair cells. Place Theory Long ago, Hermann von Helmholtz (1863) proposed that specific sound frequencies vibrate specific portions of the basilar membrane, producing distinct pitches, just as plucking specific strings on a harp produces sounds of varied pitch. This model, called place theory, holds that perception of pitch corresponds to the vibration of different portions, or places, along the basilar membrane. Place theory assumes that hair cells at various locations respond independently and that different sets of hair cells are vibrated by different sound frequencies. The brain then detects the frequency of a tone according to which area along the basilar membrane is most active. Evidence that this place coding theory is correct comes from two sources. High doses of antibiotics, such as kanamycin, can cause damage to the basilar membrane by inducing hair cell loss. This loss starts at the base of the membrane and higher frequencies are affected first (Stebbins et al., 1969). The other source of evidence is the success of cochlear implants. If a person is deaf because of the loss of basilar membrane stimulation, a cochlear implant device can be implanted that mechanically converts the sound waves into vibrations at different regions of the membrane according to the frequency. Provided that the basilar membrane and all later aspects of the auditory system are functioning normally, hearing will be restored. 11 Physiological Psychology School of Distance Education Frequency Theory Other theorists in the 19th century proposed an alternative theory of pitch perception, called frequency theory (Rutherford, 1886). Frequency theory holds that perception of pitch corresponds to the rate, or frequency, at which the entire basilar membrane vibrates. This theory views the basilar membrane as more like a drumhead than a harp. According to frequency theory, the whole membrane vibrates in unison in response to sounds. However, a particular sound frequency, say 3000 Hz, causes the basilar membrane to vibrate at a corresponding rate of 3000 times per second. The brain detects the frequency of a tone by the rate at which the auditory nerve fibers fire. The Two Theories of Hearing Combined Although the original theories had to be revised, the current thinking is that pitch perception depends on both place and frequency coding of vibrations along the basilar membrane (Goldstein, 1996). Sounds under 1000 Hz appear to be translated into pitch through frequency coding. For sounds between 1000 and 5000 Hz, pitch perception seems to depend on a combination of frequency and place coding. Sounds over 5000 Hz seem to be handled through place coding only. Again we find that theories that were pitted against each other for decades are complementary rather than contradictory. For additional reading: The volley principle (Wever and Bray, 1937) The volley principle holds that groups of auditory nerve fibers fire neural impulses in rapid succession, creating volleys of impulses. These volleys exceed the 1000 per-second limit. SENSATIONS OF TASTE AND SMELL The senses of taste and smell allow us to separate undesirable or even lethal foods from those that are pleasant to eat and nutritious. The sense of smell also allows animals to recognize the proximity of other animals or even individuals among animals. Finally, both senses are strongly tied to primitive emotional and behavioral functions of our nervous systems. Primary Sensations of Taste The identities of the specific chemicals that excite different taste receptors are not all known. Even so, psychophysiologic and neurophysiologic studies have identified at least 12 Physiological Psychology School of Distance Education 13 possible or probable chemical receptors in the taste cells. For practical analysis of taste, the aforementioned receptor capabilities have also been grouped into five general categories called the primary sensations of taste. They are sour, salty, sweet, bitter, and "umami." A person can perceive hundreds of different tastes. They are all supposed to be combinations of the elementary taste sensations, just as all the colors we can see are combinations of the three primary colors. Sour Taste. The sour taste is caused by acids, that is, by the hydrogen ion concentration, and the intensity of this taste sensation is approximately proportional to the logarithm of the hydrogen ion concentration. That is, the more acidic the food, the stronger the sour sensation becomes. Salty Taste. The salty taste is elicited by ionized salts, mainly by the sodium ion concentration. The quality of the taste varies somewhat from one salt to another, because some salts elicit other taste sensations in addition to saltiness. Sweet Taste. The sweet taste is not caused by any single class of chemicals. Some of the types of chemicals that cause this taste include sugars, glycols, alcohols, aldehydes, ketones, amides, esters, some amino acids , some small proteins, sulfonic acids, halogenated acids, and inorganic salts of lead and beryllium. Note specifically that most of the substances that cause a sweet taste are organic chemicals. It is especially interesting that slight changes in the chemical structure, such as addition of a simple radical, can often change the substance from sweet to bitter. Bitter Taste. The bitter taste, like the sweet taste, is not caused by any single type of chemical agent. Here again, the substances that give the bitter taste are almost entirely organic substances. Two particular classes of substances are especially likely to cause bitter taste sensations: (1) long-chain organic substances that contain nitrogen, and (2) alkaloids. Some substances that at first taste sweet have a bitter aftertaste. This is true of saccharin, which makes this substance objectionable to some people. 13 Physiological Psychology School of Distance Education The bitter taste, when it occurs in high intensity, usually causes the person or animal to reject the food. This is undoubtedly an important function of the bitter taste sensation, because many deadly toxins found in poisonous plants are alkaloids, and virtually all of these cause intensely bitter taste, usually followed by rejection of the food. Umami Taste. Umami is a Japanese word (meaning "delicious") designating a pleasant taste sensation that is qualitatively different from sour, salty, sweet, or bitter. Umami is the dominant taste of food containing L-glutamate, such as meat extracts and aging cheese, and some physiologists consider it to be a separate, fifth category of primary taste stimuli. Taste Blindness. Some people are taste blind for certain substances, especially for different types of thiourea compounds. A substance used frequently by psychologists for demonstrating taste blindness is phenylthiocarbamide, for which about 15 to 30 per cent of all people exhibit taste blindness; the exact percentage depends on the method of testing and the concentration of the substance. Taste Bud and Its Function A taste bud has a diameter of about 1/30 millimeter and a length of about 1/16 millimeter. The taste bud is composed of about 50 modified epithelial cells, some of which are supporting cells called sustentacular cells and others of which are taste cells. The taste cells are continually being replaced by mitotic division of surrounding epithelial cells, so that some taste cells are young cells. Others are mature cells that lie toward the center of the bud; these soon break up and dissolve. The life span of each taste cell is about 10 days in lower mammals but is unknown for humans. The outer tips of the taste cells are arranged around a minute taste pore. From the tip of each taste cell, several microvilli, or taste hairs, protrude outward into the taste pore to approach the cavity of the mouth. These microvilli provide the receptor surface for taste. Interwoven around the bodies of the taste cells is a branching terminal network of taste nerve fibers that are stimulated by the taste receptor cells. Some of these fibers invaginate into folds of the taste cell membranes. Many vesicles form beneath the cell 14 Physiological Psychology School of Distance Education membrane near the fibers. It is believed that these vesicles contain a neurotransmitter substance that is released through the cell membrane to excite the nerve fiber endings in response to taste stimulation. Location of the Taste Buds. The taste buds are found on three types of papillae of the tongue, as follows: (1) A large number of taste buds are on the walls of the troughs that surround the circumvallate papillae, which form a V line on the surface of the posterior tongue. (2) Moderate numbers of taste buds are on the fungiform papillae over the flat anterior surface of the tongue. (3) Moderate numbers are on the foliate papillae located in the folds along the lateral surfaces of the tongue. Additional taste buds are located on the palate, and a few are found on the tonsillar pillars, on the epiglottis, and even in the proximal esophagus. Adults have 3000 to 10,000 taste buds, and children have a few more. Beyond the age of 45 years, many taste buds degenerate, causing the taste sensation to become progressively less critical in old age. Specificity of Taste Buds for a Primary Taste Stimulus. Microelectrode studies from single taste buds show that each taste bud usually responds mostly to one of the five primary taste stimuli when the taste substance is in low concentration. But at high concentration, most buds can be excited by two or more of the primary taste stimuli, as well as by a few other taste stimuli that do not fit into the "primary" categories. Mechanism of Stimulation of Taste Buds Receptor Potential. The membrane of the taste cell, like that of most other sensory receptor cells, is negatively charged on the inside with respect to the outside. Application of a taste substance to the taste hairs causes partial loss of this negative potential-that is, the taste cell becomes depolarized. In most instances, the decrease in potential, within a wide range, is approximately proportional to the logarithm of concentration of the stimulating substance. This change in electrical potential in the taste cell is called the receptor potential for taste. The mechanism by which most stimulating substances react with the taste villi to initiate 15 Physiological Psychology School of Distance Education the receptor potential is by binding of the taste chemical to a protein receptor molecule that lies on the outer surface of the taste receptor cell near to or protruding through a villus membrane. This, in turn, opens ion channels, which allows positively charged sodium ions or hydrogen ions to enter and depolarize the normal negativity of the cell. Then the taste chemical itself is gradually washed away from the taste villus by the saliva, which removes the stimulus. The type of receptor protein in each taste villus determines the type of taste that will be perceived. For sodium ions and hydrogen ions, which elicit salty and sour taste sensations, respectively, the receptor proteins open specific ion channels in the apical membranes of the taste cells, thereby activating the receptors. However, for the sweet and bitter taste sensations, the portions of the receptor protein molecules that protrude through the apical membranes activate second-messenger transmitter substances inside the taste cells, and these second messengers cause intracellular chemical changes that elicit the taste signals. Adaptation of Taste Everyone is familiar with the fact that taste sensations adapt rapidly, often almost completely within a minute or so of continuous stimulation. Yet, from electrophysiological studies of taste nerve fibers, it is clear that adaptation of the taste buds themselves usually accounts for no more than about half of this. Therefore, the final extreme degree of adaptation that occurs in the sensation of taste almost certainly occurs in the central nervous system itself, although the mechanism and site of this are not known. At any rate, it is a mechanism different from that of most other sensory systems, which adapt almost entirely at the receptors. The phenomenon of taste preference almost certainly results from some mechanism located in the central nervous system and not from a mechanism in the taste receptors themselves, although it is true that the receptors often become sensitized in favor of a needed nutrient. Gustatory information is conveyed along cranial nerves to the nucleus of the solitary tract in the medulla. From there, neurons travel to the thalamus, and from there to the primary sensory region of the cerebral cortex, the amygdale and the hypothalamus. Smell Smell is the least understood of our senses. This results partly from the fact that the sense of smell is a subjective phenomenon that cannot be studied with ease in lower 16 Physiological Psychology School of Distance Education animals. Another complicating problem is that the sense of smell is poorly developed in human beings in comparison with the sense of smell in many lower animals. Olfactory Membrane The olfactory membrane lies in the superior part of each nostril. Medially, the olfactory membrane folds downward along the surface of the superior septum; laterally, it folds over the superior turbinate and even over a small portion of the upper surface of the middle turbinate. In each nostril, the olfactory membrane has a surface area of about 2.4 square centimeters. Olfactory Cells. The receptor cells for the smell sensation are the olfactory cells, which are actually bipolar nerve cells derived originally from the central nervous system itself. There are about 100 million of these cells in the olfactory epithelium interspersed among sustentacular cells. The mucosal end of the olfactory cell forms a knob from which 4 to 25 olfactory hairs (also called olfactory cilia), measuring 0.3 micrometer in diameter and up to 200 micrometers in length, project into the mucus that coats the inner surface of the nasal cavity. These projecting olfactory cilia form a dense mat in the mucus, and it is these cilia that react to odors in the air and stimulate the olfactory cells. Spaced among the olfactory cells in the olfactory membrane are many small Bowman's glands that secrete mucus onto the surface of the olfactory membrane. Stimulation of the Olfactory Cells Mechanism of Excitation of the Olfactory Cells. The portion of each olfactory cell that responds to the olfactory chemical stimuli is the olfactory cilia. The odorant substance, on coming in contact with the olfactory membrane surface, first diffuses into the mucus that covers the cilia. Then it binds with receptor proteins in the membrane of each cilium. Each receptor protein is actually a long molecule that threads its way through the membrane about seven times, folding inward and outward. The odorant binds with the portion of the receptor protein that folds to the outside. The inside of the folding protein, however, is coupled to a so-called G-protein, itself a combination of three subunits. On excitation of the receptor protein, an alpha subunit breaks away from the G-protein and immediately activates adenylyl cyclase, which is attached to the inside of the ciliary membrane near the receptor cell body. The activated cyclase, in turn, converts many molecules of intracellular adenosine triphosphate into cyclic adenosine monophosphate (cAMP). Finally, this cAMP activates another nearby membrane protein, a gated sodium ion channel, that opens its "gate" and allows large numbers of sodium 17 Physiological Psychology School of Distance Education ions to pour through the membrane into the receptor cell cytoplasm. The sodium ions increase the electrical potential in the positive direction inside the cell membrane, thus exciting the olfactory neuron and transmitting action potentials into the central nervous system by way of the olfactory nerve. The importance of this mechanism for activating olfactory nerves is that it greatly multiplies the excitatory effect of even the weakest odorant. To summarize, the process works as follows: (1) Activation of the receptor protein by the odorant substance activates the G-protein complex. (2) This, in turn, activates multiple molecules of adenylyl cyclase inside the olfactory cell membrane. (3) This causes the formation of many times more molecules of cAMP. (4) Finally, the cAMP opens still many times more sodium ion channels. Therefore, even the most minute concentration of a specific odorant initiates a cascading effect that opens extremely large numbers of sodium channels. This accounts for the exquisite sensitivity of the olfactory neurons to even the slightest amount of odorant. In addition to the basic chemical mechanism by which the olfactory cells are stimulated, several physical factors affect the degree of stimulation. First, only volatile substances that can be sniffed into the nostrils can be smelled. Second, the stimulating substance must be at least slightly water soluble so that it can pass through the mucus to reach the olfactory cilia. Third, it is helpful for the substance to be at least slightly lipid soluble, presumably because lipid constituents of the cilium itself are a weak barrier to non-lipidsoluble odorants. Transmission of Smell Signals into the Central Nervous System The olfactory portions of the brain were among the first brain structures developed in primitive animals, and much of the remainder of the brain developed around these olfactory beginnings. In fact, part of the brain that originally subserved olfaction later evolved into the basal brain structures that control emotions and other aspects of human behavior; this is the system we call the limbic system. Transmission of Olfactory Signals into the Olfactory Bulb. 18 Physiological Psychology School of Distance Education The olfactory nerve fibers leading backward from the bulb are called cranial nerve I, or the olfactory tract. However, in reality, both the tract and the bulb are an anterior outgrowth of brain tissue from the base of the brain; the bulbous enlargement at its end, the olfactory bulb, lies over the cribriform plate, separating the brain cavity from the upper reaches of the nasal cavity. The cribriform plate has multiple small perforations through which an equal number of small nerves pass upward from the olfactory membrane in the nasal cavity to enter the olfactory bulb in the cranial cavity. Each bulb has several thousand glomeruli- short axons from the olfactory cells terminating in multiple globular structures within the olfactory bulb- each of which is the terminus for about 25,000 axons from olfactory cells. Each glomerulus also is the terminus for dendrites from about 25 large mitral cells and about 60 smaller tufted cells, the cell bodies of which lie in the olfactory bulb superior to the glomeruli. These dendrites receive synapses from the olfactory cell neurons, and the mitral and tufted cells send axons through the olfactory tract to transmit olfactory signals to higher levels in the central nervous system. Only about 2% of inhaled air comes in contact with the olfactory receptors, which are positioned in the nasal mucosa above the mainstream of airflow. Olfactory sensitivity can be increased by forceful sniffing, which draws the air into contact with the receptors. PAIN The receptors for pain are free nerve endings distributed throughout the skin as well as in muscles, joints and internal organs. These are called nociceptors. They respond to stimulation that damages tissues, including mechanical injury (e.g. cutting, crushing), chemical damage (e.g. corrosive substances) and extremes of temperature (burning or freezing). Within the tissues, the nerve endings are stimulated by various chemicals produced by or released from damaged tissues. These include potassium ions from damaged cells, bradykinin from blood plasma leaking from damaged blood vessels, and histamine from mast cells, which form part of the mechanism of inflammation. Damaged cells also produce prostaglandins, which seem to sensitize nerve endings to other substances. The analgesic (pain-relieving) drug aspirin acts by preventing the synthesis of prostaglandins. Many, if not most, ailments of the body cause pain. Furthermore, the ability to diagnose different diseases depends to a great extent on a physician's knowledge of the different 19 Physiological Psychology School of Distance Education qualities of pain. Pain Is a Protective Mechanism Pain occurs whenever any tissues are being damaged, and it causes the individual to react to remove the pain stimulus. Even such simple activities as sitting for a long time can cause tissue destruction because of lack of blood flow to the skin where it is compressed by the weight of the body. When the skin becomes painful as a result of the ischemia, the person normally shifts weight subconsciously. But a person who has lost the pain sense, as after spinal cord injury, fails to feel the pain and, therefore, fails to shift. This soon results in total breakdown and desquamation of the skin at the areas of pressure. Types of Pain and Their Qualities-Fast Pain and Slow Pain Pain has been classified into two major types: fast pain and slow pain. Fast pain is felt within about 0.1 second after a pain stimulus is applied, whereas slow pain begins only after 1 second or more and then increases slowly over many seconds and sometimes even minutes. The conduction pathways for these two types of pain are different and each of them has specific qualities. Fast pain is also described by many alternative names, such as sharp pain, pricking pain, acute pain, and electric pain. This type of pain is felt when a needle is stuck into the skin, when the skin is cut with a knife, or when the skin is acutely burned. It is also felt when the skin is subjected to electric shock. Fast-sharp pain is not felt in deeper tissues of the body. Slow pain also goes by many names, such as slow burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain. This type of pain is usually associated with tissue destruction. It can lead to prolonged, unbearable suffering. It can occur both in the skin and in almost any deep tissue or organ. Pain Receptors and Their Stimulation Pain Receptors Are Free Nerve Endings The pain receptors in the skin and other tissues are all free nerve endings. They are widespread in the superficial layers of the skin as well as in certain internal tissues, such as the periosteum, the arterial walls, the joint surfaces, and the falx and tentorium in the cranial vault. Most other deep tissues are only sparsely supplied with pain endings; 20 Physiological Psychology School of Distance Education nevertheless, any widespread tissue damage can summate to cause the slow-chronicaching type of pain in most of these areas. Three Types of Stimuli Excite Pain Receptors-Mechanical, Thermal, and Chemical Pain can be elicited by multiple types of stimuli. They are classified as mechanical, thermal, and chemical pain stimuli. In general, fast pain is elicited by the mechanical and thermal types of stimuli, whereas slow pain can be elicited by all three types. Some of the chemicals that excite the chemical type of pain are bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes. In addition, prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them. The chemical substances are especially important in stimulating the slow, suffering type of pain that occurs after tissue injury. Non-adapting Nature of Pain Receptors In contrast to most other sensory receptors of the body, pain receptors adapt very little and sometimes not at all. In fact, under some conditions, excitation of pain fibers becomes progressively greater, especially so for slow-aching-nauseous pain, as the pain stimulus continues. This increase in sensitivity of the pain receptors is called hyperalgesia. One can readily understand the importance of this failure of pain receptors to adapt, because it allows the pain to keep the person apprised of a tissue damaging stimulus as long as it persists. Rate of Tissue Damage as a Stimulus for Pain The average person begins to perceive pain when the skin is heated above 45°C. This is also the temperature at which the tissues begin to be damaged by heat; indeed, the tissues are eventually destroyed if the temperature remains above this level indefinitely. Therefore, it is immediately apparent that pain resulting from heat is closely correlated with the rate at which damage to the tissues is occurring and not with the total damage that has already occurred. The intensity of pain is also closely correlated with the rate of tissue damage from causes other than heat, such as bacterial infection, tissue ischemia, tissue contusion, and so forth. 21 Physiological Psychology School of Distance Education Tissue Ischemia as a Cause of Pain When blood flow to a tissue is blocked, the tissue often becomes very painful within a few minutes. The greater the rate of metabolism of the tissue, the more rapidly the pain appears. For instance, if a blood pressure cuff is placed around the upper arm and inflated until the arterial blood flow ceases, exercise of the forearm muscles sometimes can cause muscle pain within 15 to 20 seconds. In the absence of muscle exercise, the pain may not appear for 3 to 4 minutes even though the muscle blood flow remains zero. Muscle Spasm as a Cause of Pain Muscle spasm is also a common cause of pain, and it is the basis of many clinical pain syndromes. This pain probably results partially from the direct effect of muscle spasm in stimulating mechano-sensitive pain receptors, but it might also result from the indirect effect of muscle spasm to compress the blood vessels and cause ischemia. Also, the spasm increases the rate of metabolism in the muscle tissue, thus making the relative ischemia even greater, creating ideal conditions for the release of chemical paininducing substances. Dual Pathways for Transmission of Pain Signals into the Central Nervous System Even though all pain receptors are free nerve endings, these endings use two separate pathways for transmitting pain signals into the central nervous system. The two pathways mainly correspond to the two types of pain-a fast-sharp pain pathway and a slow-chronic pain pathway. Peripheral Pain Fibers-"Fast" and "Slow" Fibers The fast-sharp pain signals are elicited by either mechanical or thermal pain stimuli; they are transmitted in the peripheral nerves to the spinal cord by small type Aδ fibers at velocities between 6 and 30 m/sec. Conversely, the slow-chronic type of pain is elicited mostly by chemical types of pain stimuli but sometimes by persisting mechanical or thermal stimuli. This slow-chronic pain is transmitted to the spinal cord by type C fibers at velocities between 0.5 and 2 m/sec. Because of this double system of pain innervation, a sudden painful stimulus often gives a "double" pain sensation: a fast-sharp pain that is transmitted to the brain by the Aδ fiber pathway, followed a second or so later by a slow pain that is transmitted by the C 22 Physiological Psychology School of Distance Education fiber pathway. The sharp pain apprises the person rapidly of a damaging influence and, therefore, plays an important role in making the person react immediately to remove himself or herself from the stimulus. The slow pain tends to become greater over time. This sensation eventually produces the intolerable suffering of long-continued pain and makes the person keep trying to relieve the cause of the pain. On entering the spinal cord from the dorsal spinal roots, the pain fibers terminate on relay neurons in the dorsal horns. Here again, there are two systems for processing the pain signals on their way to the brain. While pain information is clearly represented in the cortex (otherwise we would not be aware of it), it is not localized in the same way as tactile information. Pain information is known to be passed from the thalamus to the cingulated cortex, which is part of the limbic system. Limbic system is involved in emotional experience and behavior. Pain is usually described as having affective (emotional) as well as sensory components. Emotional and ‘higher-level’ cognitive processes can control the experience of pain. For example, if a person in acute pain is given an injection of pure water, believing it to be morphine, their pain will be dramatically relieved. This is an example of a placebo effect. Similarly, pain can be made worse by fear, for example if the sufferer believes it to result from a life-threatening illness rather than a trivial disorder. Melzack and Wall (1965) proposed a gate-control theory to explain such top-down effects on pain perception. The core of the theory is that stimulation of A fibers inhibits the firing of C fibers, thereby effectively closing a ‘gate’ for pain signals. This stimulation can come from cutaneous sensations, and is the basis for pain reduction when nearby areas of skin are strongly stimulated, for example by vigorous rubbing. The stimulation of the A fibers can also come from descending neurons from the brain, which is the route for the top-down influences of pain. One such pathway originates in the periaqueductal gray (PAG) region of the midbrain. Stimulation of the PAG reduces pain sensation. Analgesic drugs such as morphine act on receptors in the PAG. It is supposed that endorphins, which are produced by the body, reduce pain by acting on these receptors. Pain Suppression ("Analgesia") System in the Brain and Spinal Cord The degree to which a person reacts to pain varies tremendously. This results partly from a capability of the brain itself to suppress input of pain signals to the nervous 23 Physiological Psychology School of Distance Education system by activating a pain control system, called an analgesia system. The analgesia system consists of three major components: (1) The periaqueductal gray and periventricular areas of the mesencephalon and upper pons surround the aqueduct of Sylvius and portions of the third and fourth ventricles. Neurons from these areas send signals to (2) the raphe magnus nucleus, a thin midline nucleus located in the lower pons and upper medulla, and the nucleus reticularis paragigantocellularis, located laterally in the medulla. From these nuclei, second-order signals are transmitted down the dorsolateral columns in the spinal cord to (3) a pain inhibitory complex located in the dorsal horns of the spinal cord. At this point, the analgesia signals can block the pain before it is relayed to the brain. Electrical stimulation either in the periaqueductal gray area or in the raphe magnus nucleus can suppress many strong pain signals entering by way of the dorsal spinal roots. Also, stimulation of areas at still higher levels of the brain that excite the periaqueductal gray area can also suppress pain. Some of these areas are (1) the periventricular nuclei in the hypothalamus, lying adjacent to the third ventricle, and (2) to a lesser extent, the medial forebrain bundle, also in the hypothalamus. For additional reading: Referred Pain Through precise neural pathways, the brain is able to perceive the area of stimulation and project the pain sensation back to that area. The sensation of pain from certain visceral organs, however, may not be perceived as arising from those organs but from other somatic locations. This phenomenon is known as referred pain. The sensation of referred pain is relatively consistent from one person to another and is clinically important in diagnosing organ dysfunctions. The pain of a heart attack, for example, may be perceived subcutaneously over the heart and down the medial side of the left arm. Ulcers of the stomach may cause pain that is perceived as coming from the upper central (epigastric) region of the trunk. Phantom Pain Phantom pain is frequently experienced by an amputee who continues to feel pain from the body part that was amputated, as if it were still there. After amputation, the severed sensory neurons heal and function in the remaining portion of the appendage. Although it is not known why impulses that are interpreted as pain are sent periodically through these neurons, the sensations evoked in the brain are projected to the region of the amputation, resulting in phantom pain. 24 Physiological Psychology School of Distance Education TACTILE AND PRESSURE RECEPTORS Both tactile receptors and pressure receptors are sensitive to mechanical forces that distort or displace the tissue in which they are located. Tactile receptors respond to fine, or light, touch and are located primarily in the dermis and hypodermis of the skin. Pressure receptors respond to pressure, vibration, and stretch and are commonly found in the hypodermis of the skin and in the tendons and ligaments of joints. Corpuscles of Touch A corpuscle of touch (Meissner’s corpuscle) is an oval receptor composed of a mass of dendritic endings from two or three nerve fibers enclosed by connective tissue sheaths. These corpuscles are numerous in the hairless portions of the body, such as the eyelids, lips, tip of the tongue, fingertips, palms of the hands, soles of the feet, nipples, and external genitalia. Corpuscles of touch lie within the papillary layer of the dermis, where they are especially sensitive to the movement of objects that barely contact the skin. Free Nerve Endings Free nerve endings are the least modified and the most superficial of the tactile receptors. These receptors extend into the lower layers of the epidermis, where they end as knobs between the epithelial cells. Free nerve endings respond chiefly to pain and temperature, but they also detect touch and pressure, for example from clothing. Some free nerve endings are particularly sensitive to tickle and itch. Root Hair Plexuses Root hair plexuses are a specialized type of free nerve ending. They are coiled around hair follicles, where they respond to movement of the hair. Lamellated Corpuscles Lamellated (pacinian) corpuscles are large, onion-shaped receptors composed of the dendritic endings of several sensory nerve fibers enclosed by connective tissue layers. They are commonly found within the synovial membranes of synovial joints, in the perimysium of skeletal muscle tissue, and in certain visceral organs. Lamellated corpuscles are also abundant in the skin of the palms and fingers of the hand, soles of the feet, external genitalia, and breasts. They respond to heavy pressures, generally those that are constantly applied. They can also detect deep vibrations in tissues and organs. Organs of Ruffini The organs of Ruffini are encapsulated nerve endings that are found in the deep layers of the dermis and in subcutaneous tissue, where they respond to deep continuous pressure and to stretch. They are also present in joint capsules and function in the detection of joint movement. 25 Physiological Psychology School of Distance Education Bulbs of Krause The bulbs of Krause are thought to be a variation of Meissner’s corpuscles. They are most abundant in the mucous membranes, and therefore are sometimes called mucocutaneous corpuscles. Historically, both the organs of Ruffini and the bulbs of Krause have been considered to be thermoreceptors—the former heat receptors and the latter cold receptors. However, both are actually mechanoreceptors. The bulbs of Krause respond to light pressure and low-frequency vibration. Any mother can attest to the calming effect that holding and patting have on a crying baby. It has been known that the touch of massage can relieve pain and improve concentration. There is now evidence that touching and caressing newborns actually enhance their development. Massaged infants gain weight nearly 50% faster than unmassaged infants. They are also more active, alert, and responsive. Even premature infants grow and mature faster if they are regularly held and touched. Experiments with rats have shown that licking and grooming by the mother stimulate the secretion of growth hormones in her pups (young). The amount of growth hormone is significantly reduced in isolated pups that are not licked or groomed. Isolated pups that are stroked periodically with a paintbrush, however, have normal secretion of growth hormone. THERMAL SENSATIONS Thermal Receptors and Their Excitation The human being can perceive different gradations of cold and heat, from freezing cold to cold to cool to indifferent to warm to hot to burning hot. Thermal gradations are discriminated by at least three types of sensory receptors: cold receptors, warmth receptors, and pain receptors. The pain receptors are stimulated only by extreme degrees of heat or cold and, therefore, are responsible, along with the cold and warmth receptors, for "freezing cold" and "burning hot" sensations. The cold and warmth receptors are located immediately under the skin at discrete separated spots. In most areas of the body, there are 3 to 10 times as many cold spots as warmth spots, and the number in different areas of the body varies from 15 to 25 cold spots per square centimeter in the lips to 3 to 5 cold spots per square centimeter in the finger to less than 1 cold spot per square centimeter in some broad surface areas of the trunk. 26 Physiological Psychology School of Distance Education Although the existence of distinctive warmth nerve endings is quite certain, based on psychological tests, they have not been identified histologically. They are presumed to be free nerve endings, because warmth signals are transmitted mainly over type C nerve fibers at transmission velocities of only 0.4 to 2 m/sec. Conversely, a definitive cold receptor has been identified. It is a special, small type Aδ myelinated nerve ending that branches a number of times, the tips of which protrude into the bottom surfaces of basal epidermal cells. Signals are transmitted from these receptors via type Aδ nerve fibers at velocities of about 20 m/sec. Some cold sensations are believed to be transmitted in type C nerve fibers as well, which suggests that some free nerve endings also might function as cold receptors. Stimulatory Effects of Rising and Falling Temperature-Adaptation of Thermal Receptors When a cold receptor is suddenly subjected to an abrupt fall in temperature, it becomes strongly stimulated at first, but this stimulation fades rapidly during the first few seconds and progressively more slowly during the next 30 minutes or more. In other words, the receptor "adapts" to a great extent, but never 100 per cent. Thus, it is evident that the thermal senses respond markedly to changes in temperature, in addition to being able to respond to steady states of temperature. This means that when the temperature of the skin is actively falling, a person feels much colder than when the temperature remains cold at the same level. Conversely, if the temperature is actively rising, the person feels much warmer than he or she would at the same temperature if it were constant. The response to changes in temperature explains the extreme degree of heat one feels on first entering a tub of hot water and the extreme degree of cold felt on going from a heated room to the out-of-doors on a cold day. Transmission of Thermal Signals in the Nervous System In general, thermal signals are transmitted in pathways parallel to those for pain signals. On entering the spinal cord, the signals travel for a few segments upward or downward in the tract of Lissauer and then terminate mainly in laminae I, II, and III of the dorsal horns-the same as for pain. After a small amount of processing by one or more cord neurons, the signals enter long, ascending thermal fibers that cross to the opposite anterolateral sensory tract and terminate in both (1) the reticular areas of the brain stem and (2) the ventrobasal complex of the thalamus. A few thermal signals are also relayed to the cerebral somatic sensory cortex from the ventrobasal complex. Occasionally a neuron in cortical somatic sensory area I has been 27 Physiological Psychology School of Distance Education found by microelectrode studies to be directly responsive to either cold or warm stimuli on a specific area of the skin. However, removal of the entire cortical postcentral gyrus in the human being reduces but does not abolish the ability to distinguish gradations of temperature. Spatial Summation of Thermal Sensations Because the number of cold or warm endings in any one surface area of the body is slight, it is difficult to judge gradations of temperature when small skin areas are stimulated. However, when a large skin area is stimulated all at once, the thermal signals from the entire area summate. For instance, rapid changes in temperature as little as 0.01°C can be detected if this change affects the entire surface of the body simultaneously. Conversely, temperature changes 100 times as great often will not be detected when the affected skin area is only 1 square centimeter in size. SENSE OF EQUILIBRIUM Equilibrium is maintained in response to two kinds of motion: 1. Static equilibrium maintains the position of the head in response to linear movements of the body, such as starting to walk or stopping. 2. Dynamic equilibrium maintains the position of the head in response to rotational motion of the body, such as rocking (as in a boat) or turning. The perception of equilibrium occurs in the vestibular apparatus, which consists of the vestibule and the semicircular canals. Motion in these two structures is detected as follows: The vestibule is the primary detector of changes in static equilibrium. A sensory receptor called a macula is located in the walls of the saccule and utricle, the two bulblike sacs of the vestibule. A macula contains numerous receptor cells called hair cells, from which numerous stereocilia (long microvilli) and a single kinocilium (a true cilium) extend into a glycoprotein gel, the otolithic membrane. Calcium carbonate crystals called otoliths pervade the otolithic membrane, increasing its density and thus responsiveness to changes in motion. Changes in linear motion cause the otolithic membrane to move forward and backward in the utricle or up and down in the saccule. The movement of the otolithic membrane causes similar movements in the embedded stereocilia of the hair cells, which in turn initiate graded potentials. The semicircular canals are the primary detector of changes in dynamic equilibrium. The three canals, individually called the anterior, posterior, and lateral canals, are arranged at right angles to one another. The expanded base of each canal, called an ampulla, contains a sensory receptor, or crista ampullaris. Like the maculae of the vestibule, each crista contains numerous hair cells whose stereocilia and kinocilium protrude into a gelatinous matrix, the cupula (which is analogous to the otolithic 28 Physiological Psychology School of Distance Education membranes of the maculae). Changes in rotational motion cause the cupula and the embedded stereocilia to move, which stimulates the hair cell to generate a graded potential. Graded potentials in the hair cells of the maculae and cristae result in changes in the amounts of neurotransmitter secreted. In response to these changes, action potentials are generated in the fibers of the vestibular nerve, which subsequently joins the vestibulocochlear nerve. From here, the nerve impulses travel to the pons and the cerebellum. PROPRIOCEPTION Proprioceptors monitor our own movements (proprius means “one’s own”) by responding to changes in stretch and tension, and by transmitting action potentials to the cerebellum. Proprioceptor information is then used to adjust the strength and timing of muscle contractions to produce coordinated movements. Some of the sensory impulses from proprioceptors reach the level of consciousness as the kinesthetic sense, by which the position of the body parts is perceived. With the kinesthetic sense, the position and movement of the limbs can be determined without visual sensations, such as when dressing or walking in the dark. The kinesthetic sense, along with hearing, becomes keenly developed in a blind person. High-speed transmission is a vital characteristic of the kinesthetic sense because rapid feedback to various body parts is essential for quick, smooth, coordinated body movements. Proprioceptors are located in and around synovial joints, in skeletal muscle, between tendons and muscles, and in the inner ear. They are of four types: joint kinesthetic receptors, neuromuscular spindles, neurotendinous receptors, and sensory hair cells. • Joint kinesthetic receptors are located in synovial joint capsules, where they are stimulated by changes in body position as the joints are moved. • Neuromuscular spindles are located in skeletal muscle, particularly in the muscles of the limbs. They consist of the endings of sensory neurons that are spiraled around specialized individual muscle fibers. Neuromuscular spindles are stimulated by an increase in muscle tension caused by the lengthening or stretching of the individual fibers, and thus provide information about the length of the muscle and the speed of muscle contraction. • Neurotendinous receptors (Golgi tendon organs) are located where a muscle attaches to a tendon. They are stimulated by the tension produced in a tendon when the attached muscle is either stretched or contracted. • Sensory hair cells of the inner ear are located in a fluid-filled, ductule structure called the membranous labyrinth. 29 Physiological Psychology School of Distance Education MODULE 2 MUSCLES AND GLANDS Muscle enables complex movements that are either under conscious control, such as turning the pages of a book, or involuntary, such as the contraction of the heart or the peristalsis in the gut. The three types of muscles found in the human body are skeletal (striated) muscles, cardiac muscles and smooth muscles. Striated muscle All movement is the result of the contraction of muscles. The muscles that we feel under our skins, as well as many internal muscles that we cannot feel, such as the extraocular muscles that move the eyeballs, are made of contractile tissue called skeletal or striated muscle. A muscle is a bundle of numerous muscle fibers. Each muscle fiber is a single long cell, and the cells in skeletal muscle are arranged parallel to each other, but are separate. Within each fiber are numerous myofibrils, which run the full length of the fiber. The name ‘striated muscle’ comes from the striped appearance that skeletal muscle has under the microscope. The stripes consist of a number of bands and lines in each myofibril. Each set of bands and lines is a functional unit called a sarcomere. A sarcomere is composed of intersecting filaments made of proteins called actin and myosin. When a muscle is stimulated, a contraction occurs as a result of the actin filaments at each end of a sarcomere being pulled into the central myosin filaments. This shortens the muscle, and is called muscular contraction. Within each muscle are subsets of fibers, which are innervated by a single motor neuron. The motor neuron and the subset of fibers are together called a motor unit. Muscles that control fine movements, such as those controlling the fingers and eye movements, have small motor units (i.e. with few muscle fibers in each). Muscles that control gross movements such as the biceps controlling flexion of the elbow, have larger motor units. Skeletal muscles do not contract in an all-or-none manner. Stronger contraction of a muscle results from the firing of more motor neurons and hence the recruitment of more motor units. Many muscles or muscle groups form opposed pairs with other muscles. Thus, for example, the biceps, which flexes the elbow, is opposed by the triceps, which extends it. Neural control of skeletal muscle Muscles are controlled by motor neurons. When the motor neuron reaches the muscle it branches, innervating the fibers of its motor unit. Between the end of each branch of 30 Physiological Psychology School of Distance Education the neuron and the muscle fiber it innervates is a type of synapse. Acetylcholine acts as the neurotransmitter, and attaches to receptors on the motor endplate of the muscle fiber. This starts an action potential, which in turn causes muscle contraction through the myosin–actin mechanism described earlier. Each motor neuron leaves the ventral horn of the spinal cord, although, there are two main sources of stimulation of motor neurons. Each muscle contains intrafusal muscle fibers, also called muscle spindles, which are stretch receptors. When a muscle is stretched by contraction of an opposing muscle, the afferent nerve fiber serving each spindle passes information to the spinal cord. Stretch receptors in the tendons which attach muscles to bones, the Golgi tendon organs, also serve as stretch detectors, passing afferent signals to the spinal cord. However, whereas intrafusal fibers respond to passive stretch of the muscle, Golgi tendon organs respond proportionally to the tension in the muscle. Both types of receptor are involved in the reflexes we examine next. Reflexes While much of our muscular activity is controlled by the brain, many very important muscle movements are controlled by spinal reflexes. Reflexes are actions that take place automatically in response to some stimulus, and permit immediate actions without the intervention of the brain. The simplest reflex is the monosynaptic stretch reflex. The best-known example of this is the patellar reflex; the knee jerk used by physicians to test the activity of spinal nerves. In this example, striking the tendon below the knee cap (patella) stretches the quadriceps, the extensor muscle in the front of the thigh. Stretching the muscle stimulates the muscle spindles. Sensory neurons from the muscle spindles enter the dorsal root of the spinal cord, and synapse with motor neurons in the ventral root, which causes the muscle to contract. The normal function of this reflex is to cause a quick adjustment of muscle contraction when the load on the muscle is increased. It acts as a continuous feedback loop matching muscular contraction to the load on the muscle. Polysynaptic reflexes are spinal reflexes that involve more than one synapse. An example is the withdrawal or flexion reflex, when a limb is rapidly removed from a painful stimulus. In this reflex, pain receptors send signals along axons to the dorsal root of the spinal cord. These axons synapse with a number of short interneurons. These interneurons connect with several motor neurons, producing a coordinated withdrawal of the affected part of the body. However, some of the interneurons connect with motor neurons on the other side of the body, where they produce limb extension: the 31 Physiological Psychology School of Distance Education crossed extensor reflex. The importance of this is that if, for example, you stand on a pin, the resulting reflex withdrawal of that foot will be compensated by greater support in the other leg. Another type of reflex results from reciprocal innervation. This allows opposed groups of muscles to organize their contraction and relaxation, permitting coordinated actions such as walking. The simplest form of reciprocal innervations is when the flexor and extensor muscles around a joint work together. In walking, for example, the knee joint bends because the quadriceps muscle relaxes as the hamstring muscle flexes. Notice that this is not a sudden on–off action; contraction and relaxation are gradual and coordinated. The use of both legs in walking involves this reciprocal innervation, and also the alternation of the actions of the two legs by means of the crossed extensor reflex. All of this occurs without the necessity for conscious intervention. The main principles of reflexes were demonstrated around the end of the 19 th and beginning of the 20th centuries by Charles Sherrington. He showed how, in many organisms, much behavior is composed of chains of reflexes. With increasing encephalization these are increasingly controlled by brain mechanisms. Smooth muscle and cardiac muscle The actions of many internal organs are carried out by smooth muscle. Smooth muscle underlies many of the physiological changes. Amongst other places, smooth muscle is found in: the walls of blood vessels, where it is responsible for their constriction and dilation. This permits fine control of blood flow to different tissues and organs; the walls of the intestines, where it is responsible for the contractions, called peristalsis, which move food through the gastrointestinal tract; the sphincters that control filling and emptying of the gastrointestinal tract and the genitourinary tract; the iris and the lens muscles within the eye; the hair follicles of the skin, where it produces piloerection (raising of the hairs) in response to cold. Generally, smooth muscle reacts slowly to stimulation, and produces mostly longerlasting changes. Smooth muscle is innervated by both branches of the autonomic nervous system, which have opposing actions. As demands on the body vary, the parasympathetic and sympathetic nervous systems vary the contraction of the smooth muscle, matching the state of the organ to those demands. 32 Physiological Psychology School of Distance Education Cardiac, or heart, muscle is a specialized tissue that causes the heart to contract (beat), pumping blood through the blood vessels. It, too, is controlled by opposing actions of both branches of the autonomic nervous system. CONTROL OF MOVEMENT BY THE BRAIN Motor Cortex Individual movements are controlled by the primary motor cortex. This occupies the precentral gyrus, parallel to the somatosensory cortex in the postcentral gyrus. Penfield and Rasmussen (1950) showed how each part of the body is controlled by a separate area of the motor cortex, and parts capable of the most precise movements (especially the fingers and lips) have larger areas of cortex devoted to them. There are direct connections between neurons in the somatosensory cortex and in the motor cortex that serve the same parts of the body. Evarts (1974), recording from the primary motor cortex of monkeys, showed that tactile stimulation of the hand produces very rapid responses in corresponding motor neurons, presumably by way of these connections. The main inputs to the primary motor cortex come from the premotor cortex and the supplementary motor area located in the gyrus anterior to the primary motor cortex. Together, these are sometimes called the secondary motor cortex. Their function seems to be to produce movement programs: coordinated sets of movements. Through numerous connections with the primary motor cortex, these motor programs control individual movements, and produce coordinated behavior. Studies using PET scans in humans have shown that the primary and secondary motor cortices, as well as the primary somatosensory cortex, are all active both during performance of well-learned response sequences and while learning new sequences (Jenkins et al., 1994). In addition, during the learning of new sequences, but not during well-practiced ones, part of the prefrontal cortex is active. Together with lesion studies, this suggests that the planning of more complex behavior, or the construction of motor programs, takes place in the prefrontal cortex. The prefrontal cortex and the secondary motor cortex both receive inputs from areas of association cortex involved with sensory and spatial information processing. Lesions in the primary motor cortex produce paralysis of particular muscles or muscle groups. However, lesions in the other areas involved in movement produce a variety of apraxias: disorders of skilled movement not due to sensory loss or paralysis. For example, patients may be unable to walk smoothly or follow instructions to move their 33 Physiological Psychology School of Distance Education legs (limb apraxia). In construction apraxia a person may be unable to make the coordinated movements necessary to copy simple designs or complete a jigsaw puzzle. Motor pathways The contraction of muscles is controlled by motor neurons in the ventral roots of the spinal cord. The pathways by which the brain controls these motor neurons are complex, and what follows is a simplification. The pyramidal system One major pathway is the pyramidal system. In one part of this, the corticospinal tract, axons from cortical neurons pass through the brain stem and down the spinal cord before synapsing with motor neurons. Most of these axons decussate (cross to the other side) in the brain stem, the remainder do so in the part of the spinal cord where their target motor neurons are located. The other part of the pyramidal system, the corticobulbar tract, passes to the medulla where it reaches the nuclei of various cranial nerves. Most of the neurons originate in large pyramidal cells in the primary motor cortex, although many originate in the primary somatosensory cortex, and some in association areas such as the premotor cortex. Some axons in the pyramidal tract end in various sensory nuclei in the brain stem and spinal cord, and in the reticular formation. Historically, the pyramidal system was characterized as the pathway by which voluntary action is controlled; lesions confined to the pyramidal system cause paralysis of voluntary movement, while many reflexes remain intact. However, the separation of voluntary and automatic control is not actually this simple. Axons from the primary motor cortex also pass to the basal ganglia and to the cerebellum, historically considered to be involved with non-voluntary movement, both of which then feed back to the primary and secondary motor cortex. The sensory connections indicate the reliance of voluntary movement on immediate sensory feedback. The extrapyramidal system The other motor pathways have collectively been called the extrapyramidal system, and characterized as involved in automatic (non-voluntary) movement. Lesions in these tracts do not cause the loss of particular movements. Rather, patients show a variety of difficulties involving either excessive movements that interfere with voluntary actions, or slowed or limited movement that interferes with both voluntary and involuntary movements. A number of tracts carry this sort of motor information, including the vestibulospinal tracts, which originate in the brain stem, and influence the tone of limb 34 Physiological Psychology School of Distance Education muscles. They receive inputs from the vestibular system, and help to control posture and maintain eye position. The rubrospinal tract has its origin in the red nucleus high in the brain stem. This receives inputs from the primary motor cortex and from the cerebellum. The rubrospinal tract connects to motor neurons of the major limb muscles, so is involved in locomotion. The reticulospinal tracts originate in the reticular formation of the brain stem. Their functions are not well understood, but they promote certain reflexes, and help control automated actions such as walking and maintaining posture. As we have said, we cannot fully separate voluntary and involuntary components of the motor system. The whole system is one in which automatic and voluntary pathways are integrated with each other and with sensory mechanisms. The basal ganglia The basal ganglia are a group of interconnected subcortical nuclei. They include the caudate nucleus and the putamen (together called the striatum), the globus pallidus, the substantia nigra and the subthalamic nucleus. The striatum receives inputs from many parts of the cerebral cortex, particularly the primary motor cortex and the primary somatosensory cortex. In turn, the striatum projects to the globus pallidus, and has twoway connections with the substantia nigra. The globus pallidus has two-way connections with the subthalamic nucleus, and projects to the secondary and primary motor cortices by way of the thalamus. The functions of the basal ganglia are not fully worked out. In general, their effect is inhibitory on the thalamus and hence on the cortex. Destruction of parts of the basal ganglia causes characteristic, serious motor disorders. Parkinson’s disease is a condition characterized by movement disorders including a tremor when not trying to move, slowness, and difficulty starting movements. The cause of Parkinson’s disease is degeneration of dopaminergic neurons in the substantia nigra, which prevents information passing back to the striatum. Parkinson’s disease is treated by large doses of L-dopa (‘Levodopa’), a precursor of dopamine. This passes into the brain and into the remaining neurons in this circuit, enabling them to produce more dopamine to affect the striatum. Huntington’s chorea is a hereditary disease producing uncontrollable jerky movements of the face and limbs. It results from degeneration of the striatum, particularly of GABAergic neurons. It is becoming clear that the basal ganglia are also involved in emotion. For example, Schneider et al. (2003) have shown that electrical stimulation of the subthalamic 35 Physiological Psychology School of Distance Education nucleus, used as a treatment for long-term sufferers from Parkinson’s disease, increases their sense of well-being and improves their emotional memory. The cerebellum The cerebellum is a relatively large structure located in the hindbrain. It contains more neurons than the cerebral cortex, and structurally has several deep cerebellar nuclei surrounded by a cortex. The cerebellum receives inputs from the motor cortex, from the vestibular system from the special senses and from the somato-sensory system. Its outputs go to motor centers in the extrapyramidal system. Damage to the cerebellum causes serious deficits in the ability to produce smooth movement, including an ‘intention tremor’ which contrasts with the resting tremor of Parkinson’s disease. Other symptoms can include muscle weakness, lack of coordination, slurring of speech, and a staggering gait (ataxia). These all suggest that the cerebellum plays a key role in programming sequential behaviors, especially those requiring integration of external stimuli and timing. The cerebellum is involved in motor learning (Ohyama et al., 2003). More recent studies have suggested that the cerebellum is important in emotional and cognitive processes. For example, Leroi et al. (2002) reported very high rates of psychiatric illness in patients with cerebellar disease. The brain stem A large class of behaviors that fall between the intentional, voluntary movements controlled by the cerebral cortex and the reflexes controlled by the spine are programmed by various centers in the brain stem. These behaviors include the automatic processes controlled by the extrapyramidal system, such as postural changes, eye movements, breathing, walking and the like. They also include more complex, species-typical sequences of behavior that serve basic biological needs. Such preprogrammed sequences can be seen in domestic animals — for example, the stereotypical posture and movements of a hunting cat. For some of these behaviors in other species, control centers have been identified in various parts of the brain stem. For example, a region of the periaqueductal gray (PAG) produces sexual receptive behavior in female rodents. Note that, although these species-typical behaviors are preprogrammed, they are not necessarily inevitable. They are responsive both to sensory inputs and to conscious modification. They are responsive both to sensory inputs and to conscious modification. 36 Physiological Psychology School of Distance Education HORMONES AND THEIR ACTION What is a hormone? The hormone or endocrine system provides, generally, a slower means of control over the functions of the body than the nervous system. Like neurotransmitters, hormones are specialized chemicals that change the activity of cells by attaching to receptors on the cells. To emphasize the close relationships we will see between hormones and the actions of the nervous system, the endocrine system is sometimes referred to as the neuroendocrine system. Most hormones are released from specialized endocrine glands, and the rest from special cells within organs like the kidney and stomach. Wherever the hormone is released from, it usually travels to its target through the bloodstream. Hormones fall mainly into four different groups of chemicals. These are: 1. peptides and proteins; 2. amino acids; 3. fatty acids; 4. steroids. The peptides and proteins exhibit a wide variety of sizes and shapes of molecule and include insulin. The amino acids include the thyroid hormones such as thyroxine, and epinephrine, which is derived from tyrosine. The fatty acids include the prostaglandins and are made from polyunsaturated fats. Finally, the steroids include testosterone and are derived from cholesterol. These subdivisions are sometimes simplified into steroids and non-steroids. Where do hormones act? Hormones mostly travel in the bloodstream where they come into contact with all cells. However, they only have an effect once they reach their own target cells. These cells have specially adapted receptors that accept the hormone in the same ‘lock and key’ fashion that for neurotransmitters. A target cell may be receptive to just one particular hormone or to a number of different hormones. For each hormone, though, there is a specific receptor site. Most hormones travel in the bloodstream to affect a distant target organ. However, some act more locally, or even on the very cell that secreted it. To differentiate between these actions the term endocrine action is used to describe a distant action, paracrine action is used to describe a more localized action, and autocrine action is used to describe a hormone that acts on the cells that released it. 37 Physiological Psychology School of Distance Education Another noteworthy feature of hormones is their speed of action. When a neuron fires, its effects are virtually immediate as conduction is fast and the neurotransmitter substance is, to all intents and purposes, instantaneously released. By contrast, when a hormone is released it must usually travel in the bloodstream until it reaches its target destination. Add to this the fact that the release of the required hormone is sometimes only triggered by another hormone also released into the bloodstream, and the time it takes for the required hormone to finally exert its effect on the target organ can be of the order of a few minutes. Compare, for example, the speed with which you remove your hand from a hot object (neuronal) with the time it takes to induce milk ejection from a stimulated nipple (30–60 seconds). Direct integration between endocrine activity and activity of the nervous system is achieved by a group of chemicals called neurohormones. These are released by the endocrine system but have their targets in the nervous system. For example, cholecystokinin (CCK) is released by the small intestine and acts on certain brain stem nuclei. Similarly, epinephrine is released into the bloodstream by the adrenal gland and travels to the neurons of the sympathetic nervous system where it causes the sympathetic arousal. Positive and negative feedback The amount of a hormone that is present in the blood is crucial for the effective working of the endocrine system. Hormonal action needs a monitoring system so that the amount of hormone can be increased or reduced as necessary. Most hormonal control is by negative feedback. The cells that initially release the hormone are receptive to the presence of the hormone in the blood. As more and more of the hormone is released, the quantity in the blood rises. At some cut-off point, the receptorswithin the endocrine gland register that there is enough hormone circulating and turn off production and/or release of any more hormone. For some hormones, there is more than one place at which such monitoring occurs. In a few cases, the feedback system is positive. Here, the detection of the presence of the hormone in the blood triggers even more to be released. An example of this is the hormone oxytocin, released from the posterior pituitarygland. This stimulates milk secretion from the breast. The act of suckling stimulates the release of oxytocin and is a positive feedback mechanism. Major Endocrine Glands of Human Body The Pituitary Gland 38 Physiological Psychology School of Distance Education The pituitary gland has two main parts, anterior and posterior. Both have a vascular link with the hypothalamus, and the posterior pituitary has a neural connection with it. They are responsible for the release of different hormones and stimulating hormones. Most of the hormones that circulate around the body are controlled in one way or another by the pituitary gland. The hypothalamus controls hormonal release. It does so mainly by influencing the release of hormones and stimulating hormones from the pituitary gland. However, control of the anterior pituitary is by hormones released by the hypothalamus but the posterior pituitary is controlled by neuronal input from the hypothalamus. The posterior pituitary gland secretes just two hormones, oxytocin and vasopressin. The former is involved in lactation and the latter is involved in blood pressure control. Most of the hormones released by the anterior pituitary are stimulating hormones. These stimulate other glands to release their hormones into the blood. The exception here is prolactin which is a hormone that acts directly on target cells. The Adrenal Glands The adrenal glands are located above the kidneys and consist of an outer layer called the adrenal cortex and an inner core called the adrenal medulla. The medulla is made up of chromaffin cells that release epinephrine and norepinephrine when stimulated. These are released as part of the stress response. The adrenal cortex secretes three different kinds of hormones, the glucocorticoids, the mineralocorticoids and the sex steroids. The corticoids are involved in metabolism and the sex steroids are involved in secondary sexual characteristics. The Pancreas The pancreas is located at the back of the abdomen. It has cells called Islets of Langerhans that secrete its hormones into the blood. The pancreas secretes insulin and glucagon to regulate the levels of blood glucose and the storage of fats. Somatostatin is also secreted, and helps to control the secretion of insulin and glucagon. The Thyroid Gland The thyroid gland is located in the throat just below the Adam’s apple. It has a butterfly shape and secretes two hormones that regulate metabolism and have an effect in nearly all parts of the body. The parathyroid gland is located in the front of the neck, close to the thyroid gland. It is actually made up of four small glands. The thyroid gland secretes thyroxine and triiodothyronine (involved in metabolism), and calcitonin (involved in calcium regulation). The parathyroids secrete 39 Physiological Psychology School of Distance Education parathyroid hormone, which is responsible for regulating the levels of calcium and phosphate in the blood. The Ovaries The ovaries are oblong organs that lie in the pelvis at the ends of the fallopian tubes. As well as egg production, they secrete a number of hormones. The testes are glandular organs that are suspended in the scrotum. As well as producing sperm, they secrete a number of hormones. The ovaries produce estrogens and the progestins. Estrogens are involved in development, especially of the reproductive system. They are not exclusively female hormones. Progestins are concerned with reproduction itself. The testes secrete androgens, and in particular, testosterone. Testosterone is an important hormone for sexual development in the male. Other Glands and Hormones The thymus hormone secreted by thymus gland is responsible for cellular immunity. Most of its job is done shortly before birth and for a short period afterwards. The kidneys secrete three different hormones; renin, erythropoietin and 1,25dihydroxy-vitamin D3. These have a role in blood pressure, erythrocyte production and calcium balance respectively. The pineal gland secretes melatonin. This has been strongly linked with the sleep– waking cycle. It also has a role in seasonal breeding and sexual maturity. There are several hormones secreted by the gastrointestinal tract. They include gastrin, secretin, cholecystokinin, gastric inhibitory peptide and somatostatin. 40 Physiological Psychology