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Download Thin filaments - MF011 General Biology 2
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The physical interaction of protein filaments for muscle function Muscle activity is a response to input from the nervous system The action of a muscle is always to contract Vertebrate Skeletal Muscle Vertebrate skeletal muscle is characterized by a hierarchy of smaller and smaller units A skeletal muscle consists of a bundle of long fibers, each a single cell, running parallel to the length of the muscle Each muscle fiber is itself a bundle of smaller myofibrils arranged longitudinally The myofibrils are composed to two kinds of myofilaments: Thin filaments consist of two strands of actin and one strand of regulatory protein Thick filaments are staggered arrays of myosin molecules Skeletal muscle is also called striated muscle because the regular arrangement of myofilaments creates a pattern of light and dark bands The functional unit of a muscle is called a sarcomere, and is bordered by Z lines Fig. 50-25 Muscle Bundle of muscle fibers Nuclei Single muscle fiber (cell) Plasma membrane Myofibril Z lines Sarcomere TEM M line 0.5 µm Thick filaments (myosin) Thin filaments (actin) Z line Z line Sarcomere Fig. 50-25a Muscle Bundle of muscle fibers Nuclei Single muscle fiber (cell) Plasma membrane Myofibril Z lines Sarcomere Fig. 50-25b TEM M line 0.5 µm Thick filaments (myosin) Thin filaments (actin) Z line Z line Sarcomere The Sliding-Filament Model of Muscle Contraction According to the sliding-filament model, filaments slide past each other longitudinally, producing more overlap between thin and thick filaments The sliding of filaments is based on interaction between actin of the thin filaments and myosin of the thick filaments The “head” of a myosin molecule binds to an actin filament, forming a cross-bridge and pulling the thin filament toward the center of the sarcomere Glycolysis and aerobic respiration generate the ATP needed to sustain muscle contraction Fig. 50-26 Sarcomere Z M Relaxed muscle Contracting muscle Fully contracted muscle Contracted Sarcomere Z 0.5 µm Fig. 50-27-1 Thick filament Thin filaments Thin filament ATP Myosin head (lowenergy configuration Thick filament Fig. 50-27-2 Thick filament Thin filaments Thin filament ATP Myosin head (lowenergy configuration Thick filament Myosin binding sites Actin ADP Pi Myosin head (highenergy configuration Fig. 50-27-3 Thick filament Thin filaments Thin filament Myosin head (lowenergy configuration ATP Thick filament Myosin binding sites Actin ADP Pi ADP Pi Cross-bridge Myosin head (highenergy configuration Fig. 50-27-4 Thick filament Thin filaments Thin filament Myosin head (lowenergy configuration ATP ATP Thick filament Thin filament moves toward center of sarcomere. ADP Myosin head (lowenergy configuration ADP +Pi Myosin binding sites Actin Pi ADP Pi Cross-bridge Myosin head (highenergy configuration The Role of Calcium and Regulatory Proteins A skeletal muscle fiber contracts only when stimulated by a motor neuron When a muscle is at rest, myosin-binding sites on the thin filament are blocked by the regulatory protein tropomyosin Fig. 50-28 Tropomyosin Actin Troponin complex Ca2+-binding sites (a) Myosin-binding sites blocked Ca2+ Myosinbinding site (b) Myosin-binding sites exposed For a muscle fiber to contract, myosin-binding sites must be uncovered This occurs when calcium ions (Ca2+) bind to a set of regulatory proteins, the troponin complex Muscle fiber contracts when the concentration of Ca2+ is high; muscle fiber contraction stops when the concentration of Ca2+ is low Fig. 50-29 Synaptic terminal Motor neuron axon T tubule Mitochondrion Sarcoplasmic reticulum (SR) Myofibril Plasma membrane of muscle fiber Ca2+ released from SR Sarcomere Synaptic terminal of motor neuron T Tubule Synaptic cleft ACh Plasma membrane SR Ca2+ ATPase pump Ca2+ ATP CYTOSOL Ca2+ ADP Pi Fig. 50-29a Synaptic terminal T tubule Motor neuron axon Mitochondrion Sarcoplasmic reticulum (SR) Myofibril Plasma membrane of muscle fiber Sarcomere Ca2+ released from SR The stimulus leading to contraction of a muscle fiber is an action potential in a motor neuron that makes a synapse with the muscle fiber The synaptic terminal of the motor neuron releases the neurotransmitter acetylcholine Acetylcholine depolarizes the muscle, causing it to produce an action potential Fig. 50-29b Synaptic terminal of motor neuron T Tubule Synaptic cleft ACh Plasma membrane SR Ca2+ ATPase pump Ca2+ ATP CYTOSOL Ca2+ ADP Pi Nervous Control of Muscle Tension Contraction of a whole muscle is graded, which means that the extent and strength of its contraction can be voluntarily altered There are two basic mechanisms by which the nervous system produces graded contractions: Varying the number of fibers that contract Varying the rate at which fibers are stimulated In a vertebrate skeletal muscle, each branched muscle fiber is innervated by one motor neuron Each motor neuron may synapse with multiple muscle fibers A motor unit consists of a single motor neuron and all the muscle fibers it controls Recruitment of multiple motor neurons results in stronger contractions A twitch results from a single action potential in a motor neuron More rapidly delivered action potentials produce a graded contraction by summation Fig. 50-30 Spinal cord Motor unit 1 Motor unit 2 Synaptic terminals Nerve Motor neuron cell body Motor neuron axon Muscle Muscle fibers Tendon Fig. 50-31 Tension Tetanus Summation of two twitches Single twitch Action potential Time Pair of action potentials Series of action potentials at high frequency Other Types of Muscle In addition to skeletal muscle, vertebrates have cardiac muscle and smooth muscle Cardiac muscle, found only in the heart, consists of striated cells electrically connected by intercalated disks Cardiac muscle can generate action potentials without neural input In smooth muscle, found mainly in walls of hollow organs, contractions are relatively slow and may be initiated by the muscles themselves Contractions may also be caused by stimulation from neurons in the autonomic nervous system Nervous system disorders can be explained in molecular terms Disorders of the nervous system include schizophrenia, depression, Alzheimer’s disease, and Parkinson’s disease Genetic and environmental factors contribute to diseases of the nervous system Schizophrenia About 1% of the world’s population suffers from schizophrenia Schizophrenia is characterized by hallucinations, delusions, blunted emotions, and other symptoms Available treatments focus on brain pathways that use dopamine as a neurotransmitter Fig. 49-21 50 Genes shared with relatives of person with schizophrenia 12.5% (3rd-degree relative) 25% (2nd-degree relative) 50% (1st-degree relative) 100% 40 30 20 10 First cousin Individual, general population 0 Relationship to person with schizophrenia Depression Two broad forms of depressive illness are known: major depressive disorder and bipolar disorder In major depressive disorder, patients have a persistent lack of interest or pleasure in most activities Bipolar disorder is characterized by manic (high-mood) and depressive (low-mood) phases Treatments for these types of depression include drugs such as Prozac and lithium Drug Addiction and the Brain Reward System The brain’s reward system rewards motivation with pleasure Some drugs are addictive because they increase activity of the brain’s reward system These drugs include cocaine, amphetamine, heroin, alcohol, and tobacco Drug addiction is characterized by compulsive consumption and an inability to control intake Fig. 49-22 Nicotine stimulates dopaminereleasing VTA neuron. Opium and heroin decrease activity of inhibitory neuron. Cocaine and amphetamines block removal of dopamine. Cerebral neuron of reward pathway Reward system response Alzheimer’s Disease Alzheimer’s disease is a mental deterioration characterized by confusion, memory loss, and other symptoms Alzheimer’s disease is caused by the formation of neurofibrillary tangles and amyloid plaques in the brain A successful treatment in humans may hinge on early detection of amyloid plaques There is no cure for this disease though some drugs are effective at relieving symptoms Fig. 49-23 Amyloid plaque Neurofibrillary tangle 20 µm Parkinson’s Disease Parkinson’s disease is a motor disorder caused by death of dopamine-secreting neurons in the midbrain It is characterized by difficulty in initiating movements, muscle tremors, slowness of movement, and rigidity There is no cure, although drugs and various other approaches are used to manage symptoms Stem Cell–Based Therapy Unlike the PNS, the CNS cannot fully repair itself However, it was recently discovered that the adult human brain contains stem cells that can differentiate into mature neurons Induction of stem cell differentiation and transplantation of cultured stem cells are potential methods for replacing neurons lost to trauma or disease Fig. 49-24 The vertebrate nervous system is grouped into two sections, the central nervous system and the peripheral nervous system. The central nervous system consists of a. b. c. d. the brain. the brain and spinal cord. the brain, spinal cord, and spinal nerves. the brain, spinal cord, sensory neurons, and motor neurons. Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. The parasympathetic and sympathetic divisions of the autonomic nervous system control many organ functions through a. b. c. positive feedback. negative feedback. acting in opposition. Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. If increased stimulation of the parasympathetic division results in decreasing heart rate, what will happen if the sympathetic division is stimulated? a. b. c. d. no impact on heart rate cause the heart to stop beating increase the heart rate change blood pressure but not heart rate Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. What is the correct pathway of information flow through neurons while taking a test, starting with reading a question and ending with marking the correct answer? a. b. c. d. sensor, interneurons, motor neurons, sensory neurons, effector effector, sensory neurons, interneurons, motor neurons, sensor sensor, sensory neurons, interneurons, motor neurons, effector sensor, interneurons, sensory neurons, motor neurons, effector Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. A poison that specifically disables the Na+/K+ pumps is added to a culture of neurons. What effect does this eventually have on the neurons? a. b. c. d. The resting membrane potential goes to zero. The inside of the neuron would become more negative relative to the outside. The inside of the neuron would become positively charged relative to the outside. Sodium would diffuse out of the cell and potassium would diffuse into the cell. Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. For a nerve cell at its resting potential, what are the forces controlling the movement of potassium ions and their direction? a. b. c. d. e. None: K+ ions do not move across the membrane at the resting potential Electrical gradient, inward; chemical gradient, inward Electrical gradient, outward; chemical gradient, inward Electrical gradient, inward; chemical gradient, outward Electrical gradient, outward; chemical gradient, outward Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. A(n) ___ in Na+ permeability and/or a(n) ___ in K+ permeability across a neuron’s plasma membrane would cause a shift in the membrane potential from -70 mV to -80mV. a. b. c. d. increase; increase increase; decrease decrease; increase decrease; decrease Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. Which of the following choices best describes what is happening at step four in the graph below? a. b. c. d. e. Some Na channels close. Most Na channels open. Some K channels close. Most K channels open. Na/K pumps are inactivated. Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. Which of the following will be the slowest at conducting an action potential? a. b. c. d. e. Large diameter, unmyelinated axon Small diameter, unmyelinated axon Myelinated axon Options a and c above No difference among these Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. Ethylene glycol tetraacetic acid (EGTA) is a chelating agent that binds to Ca2+. What effect would injecting EGTA at a synaptic terminal have on the transmission of an action potential to a post-synaptic neuron? a. b. c. d. The release of neurotransmitters by the presynaptic neuron would increase. The release of neurotransmitters by the presynaptic neuron would decrease. EGTA would block the binding of neurotransmitters in the post-synaptic neuron. The lack of Ca2+ would keep the ligand-gated ion channels open on the post-synaptic neurons. Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. Organophosphate pesticides work by inhibiting acetylcholine esterase, an enzyme that breaks down the neurotransmitter acetylcholine. Which of the following would best describe the effect of these pesticides on skeletal muscle cells? a. b. c. d. EPSPs would increase because acetylcholine would remain in the synaptic cleft longer. IPSPs would decrease because acetylcholine would remain in the synaptic cleft longer. EPSPs would decrease because acetylcholine would prevent ligand-gated ion channels from opening. IPSPs would increase because excess acetylcholine would cause Cl- channels to open. Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. Schizophrenia appears to be related to specific genetic mutations. Based on the table of genetic relatedness, who is more likely to have schizophrenia: the nephew/niece or child of a schizophrenic? a. b. nephew/niece child Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings. Schizophrenia appears to be related to specific genetic mutations. Based on the table of genetic relatedness, who is more likely to have schizophrenia: the child or parent of a schizophrenic? a. b. c. Child Parent equally likely Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings.
