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Copyright © Allyn & Bacon 2010 Chapter 9 Copyright © Allyn & Bacon 2010 Lecture Preview A Physiological and Behavioral Description of Sleep Disorders of Sleep Insomnia Narcolepsy REM sleep behavior disorder Problems associated with SWS Why Do We Sleep? Physiological Mechanisms of Sleep and Waking Biological Clocks Lecture Preview A Physiological and Behavioral Description of Sleep Disorders of Sleep Why Do We Sleep? Functions of SWS Functions of REM sleep Sleep and Learning Physiological Mechanisms of Sleep and Waking Biological Clocks Functions of Sleep Sleep is universal among vertebrates Only warm-blooded vertebrates (mammals & birds) exhibit REM Sleep appears to be essential for life Bottlenose dolphin Extremely motivating to sleep – suggests a necessity of life Copyright © Allyn & Bacon 2010 5 Copyright © Allyn & Bacon 2010 6 Copyright © Allyn & Bacon 2010 7 Functions of SWS Sleep deprivation studies with humans Sleep does not appear to play a role in rest and recuperation of body Sleep deprivation does not interfere with people’s ability to perform physical exercise No evidence of physiological stress response to sleep deprivation Deficits in cognitive abilities Perceptual distortions, hallucinations, trouble concentrating on mental tasks Copyright © Allyn & Bacon 2010 8 Functions of SWS Sleep deprivation studies with humans Once sleep deprived Ss are allowed to sleep, they never regain the total sleep they lost 7% of stages 1 and 2, 68% of SWS, 53% of REM Appears that the brain rests during sleep SWS may destroy free radicals Fatal familial insomnia (related to mad cow disease) Deficits in attention and memory Dreamlike, confused state, loss of control of ANS, insomnia, fatal Copyright © Allyn & Bacon 2010 9 Functions of SWS Studies with lab animals Sleep deprivation is fatal Not sure why Effects of exercise on SWS Not related Effects of brain activity on SWS Increased SWS following cognitive task Copyright © Allyn & Bacon 2010 10 Functions of REM Sleep Intense physiological activity Eyes dart, heart rate accelerates/decelerates, breathing becomes irregular, brain becomes more active As REM deprivation persists, pressure to enter REM builds up After several days of REM deprivation - rebound phenomenon When allowed to sleep, greater than normal percentage of time in REM sleep Important in neural development Premature infants, REM begins ~ 30 weeks, peaks ~ 40 weeks ~ 70% of newborn sleep is REM, at 6 months – 30%, late adulthood – 15% Why is it still present post-development? Learning and memory 11 Sleep and Learning Sleep aids in the consolidation of long-term memories. REM sleep facilitates the consolidation of nondeclarative memory. Slow-wave sleep facilitates the consolidation of declarative memory. Two Categories of Memory Declarative/Explicit - conscious recollection of facts & events (semantic & episodic memories) Nondeclarative/Implicit - experience can alter behavior without us being consciously aware of exactly what we have learned Categories of Memory Memory Declarative or Explicit Facts Events Nondeclarative or Implicit Skills Habits Priming Classical Nonassociative Conditioning Learning Sleep and Learning REM sleep facilitates the consolidation of nondeclarative memory. Ss learn a nondeclarative visual discrimination task at 9am Test – 7pm Some Ss took a 90 min nap – EEG Ss with no nap < Ss with SWS < Ss with REM Sleep and Learning Peigneux et al, 2004 Ss (humans) learned their way around a computerized virtual-reality town Hippocampus-dependent fMRI – same regions of the hippocampus were activated during route learning and during SWS the following night Although people who are awakened during SWS seldom report dreaming, sleeping brain rehearses information that was acquired during the previous day Consistent with animal data 16 Lecture Preview A Physiological and Behavioral Description of Sleep Disorders of Sleep Why Do We Sleep? Physiological Mechanisms of Sleep and Waking Chemical control of sleep Neural control of arousal Neural control of SWS Neural control of REM Biological Clocks Chemical Control of Sleep Sleep is regulated – by what? If deprived of SWS or REM, animal will make up for at least part of the missed sleep Amount of SWS during daytime nap is deducted from the amount of SWS that night Adenosine (nucleoside) – primary role in the control of sleep Copyright © Allyn & Bacon 2010 18 Chemical Control of Sleep Adenosine Astrocytes maintain a small stock of glycogen Increased brain activity – glycogen is converted to fuel for neurons (glucose) Prolonged wakefulness causes a decrease in glycogen in brain Fall in glycogen causes an increase in extracellular adenosine Inhibitory effect on neural activity Accumulation of adenosine – sleep promoting substance 19 Chemical Control of Sleep Adenosine During SWS, neurons rest, astrocytes renew stock of glycogen If wakefulness is prolonged, more adenosine accumulates, inhibits neural activity Produces cognitive and emotional effects of sleep deprivation Caffeine blocks adenosine receptors Copyright © Allyn & Bacon 2010 20 Adenosine Genetic factors affect the typical duration a person spends in SWS Variability in the gene that encodes for adenosine deaminase (enzyme that aids in breakdown on adenosine) People with G/A allele for this gene (breaks down adenosine more slowly), spent ~ 30 more min in SWS than people with G/G allele (more common0 Copyright © Allyn & Bacon 2010 21 Lecture Preview A Physiological and Behavioral Description of Sleep Disorders of Sleep Why Do We Sleep? Physiological Mechanisms of Sleep and Waking Chemical control of sleep Neural control of arousal Neural control of SWS Neural control of REM Biological Clocks Neural Arousal Alertness can vary, regardless of sleepiness 5 NTs play a role in alertness and wakefulness: ACh NE 5-HT Histamine Orexin Copyright © Allyn & Bacon 2010 23 Acetylcholine (ACh) 3 groups of ACh neurons Pons Activation & cortical desynchrony Basal forebrain Medial septum Controls activity of hippocampus (basal forebrain) Copyright © Allyn & Bacon 2010 24 Neural Control of Arousal ACh ACh agonists increase EEG signs of cortical arousal ACh antagonists decrease them High levels of ACh in hippocampus and neocortex during REM and waking, low during SWS 25 Neural Control of Arousal NE Locus coeruleus – located in dorsal pons Copyright © Allyn & Bacon 2010 26 NE Most neuron that release NE do not do so at terminal buttons but through axonal varicosities Axonal Varicosities – beadlike swellings of the axonal branches, contains synaptic vesicles and releases a neurotransmitter or neuromodulator. Neural Control of Arousal NE Activity of NE neurons was closely related to behavioral arousal Firing rate was high during wakefulness, low during SWS, almost zero during REM Within a few seconds of awakening, firing rate increased dramatically Increase vigilance – ability to pay attention to stimuli in the environment Copyright © Allyn & Bacon 2010 28 NE Carter et al., (2010) used viral vector to insert genes for ChR2 and NpHR (photosensitive proteins), into NE cells of LC Exposure of ChR2 to blue light activates the neurons Exposure of NpHR to yellow light inhibits the neurons Stimulation of the neurons caused immediate waking, inhibition decreased wakefulness and increased SWS Copyright © Allyn & Bacon 2010 29 Neural Control of Arousal 5-HT Stimulation of RN causes locomotion and cortical arousal PCPA (antagonist) – reduces cortical arousal Neurons most active during waking Firing rate decline during SWS Zero during REM Facilitate continuous, automatic movements Copyright © Allyn & Bacon 2010 30 Neural Control of Arousal Histamine Cell bodies located in the tuberomammillary nucleus (TMN) of the hypothalamus Connections to cortex – increase cortical activation and arousal Activity of histamine neurons is high during waking, low during SWS and REM Histamine antagonists decrease waking, increase sleep Antihistamines Copyright © Allyn & Bacon 2010 31 Neural Control of Arousal Orexin (hypocretin) Cells bodies located in lateral hypothalamus ~7000 orexin neurons – project to almost every part of brain Excitatory Orexin neurons fired at a high rate during alert or active waking and at a low rate during quiet waking, SWS and REM Copyright © Allyn & Bacon 2010 32 Lecture Preview A Physiological and Behavioral Description of Sleep Disorders of Sleep Why Do We Sleep? Physiological Mechanisms of Sleep and Waking Chemical control of sleep Neural control of arousal Neural control of SWS Neural control of REM Biological Clocks Neural Control of SWS What controls activity of arousal neurons? Preoptic area (POA) – control of sleep Contains neurons whose axons inhibit arousal neurons Destruction of POA produced total insomnia in rats Animals fell into a comma and died (3 days) Stimulation produced signs of drowsiness, sleep Ventrolateral POA (vlPOA) Damage suppresses sleep, increased Fos during sleep Release GABA – send axons to orexin, ACh, NE, 5-HT, histamine neurons 34 Neural Control of SWS POA neurons receive inhibitory input histamine, 5- HT, NE neurons Mutual inhibition may control sleep/wake periods Copyright © Allyn & Bacon 2010 35 Figure 9.14 Copyright © Allyn & Bacon 2010 Neural Control of SWS Flip-flop advantage – quick switches from one state to the other Flip-flop disadvantage – they can be unstable Narcolepsy – great difficulty remaining awake, trouble remaining asleep Orexin neurons help stabilize the sleep/wake flip-flop through excitatory connections to the wakefulness neurons Copyright © Allyn & Bacon 2010 37 Figure 9.15 Role of Orexinergic Neurons in Sleep Copyright © Allyn & Bacon 2010 Neural Control of SWS Target mutation of orexin neurons Normal amounts of sleep and waking Orexin not directly involved in regulating total amount of time spent in sleep/wake Animals bouts of wakefulness and SWS were very brief narcoplepsy Biological clock controls rhythms of sleep/wake Also receive signals from neurons that monitor nutritional state Hunger-related signals activate orexin neurons, satiety inhibits them Orexin neurons maintain arousal during the times when an 39 animal should search for food LECTURE PREVIEW A Physiological and Behavioral Description of Sleep Disorders of Sleep Why Do We Sleep? Physiological Mechanisms of Sleep and Waking Chemical control of sleep Neural control of arousal Neural control of SWS Neural control of REM Biological Clocks NEURAL CONTROL OF REM SLEEP REM sleep is controlled by a flip/flop • Controls cycles of REM & SWS Similar to the one that controls sleep/wake Copyright © Allyn & Bacon 2010 41 Neural Control of REM Sleep Sublaterodorsal Nucleus (SLD) – region of the dorsal pons containing REM-ON cells. Ventrolateral Periaqueductal Gray Matter (vlPAG) – region of the dorsal midbrain containing REM-OFF cells. Copyright © Allyn & Bacon 2010 NEURAL CONTROL OF REM SLEEP REM-On and REM-OFF regions are connected by inhibitory GABAergic neurons • • • • Stimulation of REM-ON region – REM Inhibition of REM-ON region – disrupts REM Stimulation of REM-OFF region – suppresses REM Inhibition of REM-OFF region – increase REM 43 NEURAL CONTROL OF REM SLEEP During waking, REM-OFF region receives excitatory input from orexinergic (ORXN) neurons of LH • NE & 5-HT When sleep/wake switches to sleep, SWS begins • • Activity of excitatory ORXN, NE, & 5-HT inputs to REM-OFF region decrease REM begins Internal clock – pons? • Controls alternating periods of REM and SWS 44 Figure 9.20 REM Sleep Copyright © Allyn & Bacon 2010 NEURAL CONTROL OF REM SLEEP Degeneration of orexin neurons causes narcolepsy Daytime sleepiness and fragmented sleep occur without orexin, sleep/wake flip-flop becomes unstable Orexin normally keeps REM-OFF Without orexin, emotional episodes (activate amygdala) turn REM-ON (cataplexy) • When people with cateplexy watched humorous photos, hypothalamus was activated less, amygdala was activated more (than controls) Loss of orexin neurons removed an inhibitory influence of hypothalamus on amygdala 46 Figure 9.20 REM Sleep Copyright © Allyn & Bacon 2010 NEURAL CONTROL OF REM SLEEP Neurons responsible for muscular paralysis are located just ventral to REM-ON region (SLD) Axons project to spinal cord, excite inhibitory interneurons which synapse onto motor neurons When REM flip-flop is on – motor neurons in spinal cord become inhibited (don’t respond to motor cortex) Damage to REM-ON region removes inhibition – acts out dreams See figure 9.23 Copyright © Allyn & Bacon 2010 48 NEURAL CONTROL OF REM SLEEP Neurons in SLD (REM-ON) region also send axons to: Thalamus • Control of cortical arousal Glutamatergic neurons in medial pons RF – ACh neurons of basal forebrain • Arousal and cortical desynchrony ACh neurons to tectum • Rapid eye movements Copyright © Allyn & Bacon 2010 49 LECTURE PREVIEW A Physiological and Behavioral Description of Sleep Disorders of Sleep Why Do We Sleep? Physiological Mechanisms of Sleep and Waking Biological Clocks Circadian rhythms and zeitebers The suprachiasmatic nucleus (SCN) Control of Seasonal Rhythms: the pineal gland and melatonin Changes in circadian rhythms: shift work and jet lag Biological Clocks Circadian Rhythms and Zeitgebers • • Circadian Rhythms – daily rhythmical change in behavior or physiological process. Zeitgebers – stimulus that resets the biological clock responsible for circadian rhythms. • Maintains 24 hour clock • If our biological clock runs free (in the case of constant illumination), cycle ~25 hours BIOLOGICAL CLOCKS The Suprachiasmatic Nucleus (SCN) • • • A hypothalamic nucleus containing the biological clock for many of the body’s circadian rhythms. Lesions disrupt circadian rhythms of wheel running, drinking, and hormonal secretions Provides primary control over the timing of sleep cycles • Lesions disrupt sleep pattern – sleep occurs in random bouts dispersed throughout day and night • Same amount of sleep 52 BIOLOGICAL CLOCKS SCN • • • Light is the primary zeitgeber for most activity cycles Direct projection from retina to SCN • Retinohypothalamic pathway Special photoreceptor that provides info about the ambient level of light that synchronizes circadian rhythms • Photochemical – melanopsin (ganglion cells, not rods/cones) 53 BIOLOGICAL CLOCKS How does SCN control sleep/wake cycle? SCN project to subparaventricular zone (SPZ) – dorsal to SCN SPZ DMH vlPOA & Orexin in LH Projections to vlPOA are inhibitory – inhibit sleep Projections to orexin neurons in LH are excitatory – promote wakefulness Activity of connections vary across day/night cycle Figure 9.26 Copyright © Allyn & Bacon 2010 54 Biological Clocks Control of Seasonal Rhythms: The Pineal Gland and Melatonin Pineal Gland – gland attached to the dorsal tectum; produces melatonin and plays a role in circadian and seasonal rhythms. SCN make indirect connections with PVN, spinal cord, pineal gland In response to input from SCN, pineal gland secretes melatonin during the night Melatonin acts back on various brain areas (including SCN), and controls hormones, physiological process, behaviors that show seasonal variations Biological Clocks Changes in Circadian Rhythms: • • • • • Abrupt changes in daily rhythms desynchronizes internal circadian rhythms controlled by the SCN. • E.g., Shift Work and Jet Lag This desynchronization produces sleep disturbances and mood changes, disrupts functioning during normal waking hours. People adapt more rapidly if artificial light is kept bright in the workplace and if the bedroom is kept dark Melatonin at appropriate time (just before going to bed) reduces the adverse effects of jet lag and shift work Also improved sleep of blind people • light cannot serve as a zeiteber