Brain & Behaviour Week 8 Sleep Lecture Notes PDF

Brain & Behaviour PSYC11212 Week 8 Sleep Dr Annie Pye [email protected] Brain & Behaviour PSYC11212 Week 8 Sleep Dr Annie Pye [email protected] Learning outcomes 1. Describe the course of a night’s sleep: its stages and their characteristics. 2. Discuss research on t...

Brain & Behaviour PSYC11212 Week 8 Sleep Dr Annie Pye [email protected] Brain & Behaviour PSYC11212 Week 8 Sleep Dr Annie Pye [email protected] Learning outcomes 1. Describe the course of a night’s sleep: its stages and their characteristics. 2. Discuss research on the effects of REM sleep and slow -wave sleep on learning. 3. Evaluate evidence that the onset and amount of sleep is chemically controlled, and describe the neural control of arousal. 4. Discuss the neural control of slow -wave sleep, including the sleep/waking flip -flop and the role of orexinergic neurons. 5. Discuss the neural control of REM sleep, including the REM sleep flip -flop. Lecture outline • What is sleep? – Measuring physiological responses associated with wakefulness and sleep – Stages of sleep & EEG activity • Neural basis of arousal and sleep BREAK • Dreams, nightmares and lucid dreaming • Why do we sleep? • Disorders of sleep What is sleep? • Sleep is a behaviour • Vital for normal functioning, health, well -being, and memory. • Sleep is regulated – if deprived of sleep, we will make up at least part of the sleep when permitted to do so. • Sleep research is conducted in a sleep lab. • Researchers monitor the: Electroencephalogram (EEG) – brain activity Electromyogram (EMG) – muscle activity Electro -oculogram (EOG) – eye movements Measuring physiological responses during sleep Wakefulness/Alertness • Two basic patterns of brain activity - Alpha and Beta Activity • Alpha activity - regular, medium -frequency waves of 8 -12Hz (resting quietly) • Beta activity – Irregular, mostly low -amplitude waves of 13 - 30Hz (alert and attentive) Stages of sleep • We pass through different stages of sleep every night • Moving from wakefulness to non -rapid eye movement, through slow - wave (deep) sleep to rapid eye movement (REM) sleep Stages of sleep Stage 1 Sleep • Become drowsy, enter stage one • Theta activity 3.5 – 7.5Hz • Firing of neurons in the neocortex becoming more synchronised • Transition between sleep and wakefulness • Lasts approximately 10 minutes • Irregular EEG during this stage • Theta activity like in Stage 1 • Sleep Spindles – short bursts of waves of 12 -14Hz that occur between 2 and 5 times a minute during sleep • K Complexes – sudden sharp waveforms usually only found in Stage 2 • K Complexes are associated with consolidation of memories and increased numbers of sleep spindles are associated with higher scores on intelligence tests Stage 2 Sleep • High amplitude delta activity – Slower than 3.5 Hz • Distinction – Stage 3 sees 30 -50% delta activity; stage 4 over 50% delta activity • Slow wave oscillations <1Hz – Down state and up state Stage 3 & 4 Slow Wave Sleep • EEG Desynchrony – rapid, irregular waves • This is the stage of sleep in which we dream • Profound loss of muscle tone – paralysis • If woken the person will usually appear attentive and alert • Cerebral blood flow and oxygen consumption are accelerated • Mechanisms that regulate body temperature stop working REM sleep Principal characteristics of REM and Slow -Wave Sleep REM Sleep Slow -Wave Sleep Electroencephalography desynchrony (rapid, irregular waves) Electroencephalography synchrony (slow waves) Lack of muscle tonus Moderate muscle tonus Rapid eye movements Slow or absent eye movements Penile erection or vaginal secretion Lack of genital activity Dreams Lecture outline • What is sleep? – Measuring physiological responses associated with wakefulness and sleep – Stages of sleep & EEG activity • Neural basis of arousal and sleep BREAK • Dreams, nightmares and lucid dreaming • Why do we sleep? • Disorders of sleep Neural Basis of Arousal • There are 5 different neurotransmitters that play a role in arousal (alertness and wakefulness) ➢ Acetylcholine – levels high in the hippocampus and neocortex (Marrosu et al. 1995) – activating AcH neurons in the basal forebrain causes wakefulness (Cape and Jones, 2000) ➢ Norepinephrine – Activity of noradrenergic locus coeruleus neurons increases vigilance – Increase during wakefulness – Moment -to -moment activity of noradrenergic LC neurons related to performance on tasks requiring vigilance Pons Neural Basis of Arousal ➢ Serotonin – Involved in numerous processes – Stimulation of raphe nulcei (where most of the serontenergic neurons are found) causes locomotion and cortical arousal (Peck & Vanderwolf , 1991) Neural Basis of Arousal ➢ Serotonin • Serotonergic neurons are most active during waking, steadily decline during sleep to almost zero activity in REM sleep. • Temporarily become very active after REM sleep. Neural Basis of Arousal ➢ Histamine – Histaminergic neurons are located in the hypothalamus – Drugs that prevent the synthesis of histamine or block histamine receptors decrease waking and increase sleep (Lin et al., 1998) – Activity of histaminergic neurons is high during waking and low during slow -wave and REM sleep Neural Basis of Arousal ➢ Orexin – Cell bodies that secrete orexin (also called hypocretin ) are located in the hypothalamus – Excitatory effect in the cerebral cortex and all other regions involved in arousal and wakefulness – Activating neurons in the lateral hypothalamus of mice awakens the animals from REM and non -REM sleep Neural Basis of Arousal ➢ Orexin • Orexinergic neurons in rats fire fastest in active waking, particularly when exploring and fire less frequently during quiet waking and sleep Neural Basis of Arousal Neural Control of Slow - Wave Sleep • Sleep is controlled by 3 factors – homeostatic, allostatic , and circadian • Primary homeostatic factor – presence or absence of adenosine. • Allostatic control is mediated by hormonal and neural responses to stressful situations • So if a high level of activity in the arousal related neurons keeps us awake and a low level puts us to sleep, what controls the activity of these neurons? • Inhibition of the arousal system is necessary for sleep • Group of GABAnergic neurons in the ventrolateral preoptic area ( vlPOA ) become active and supress activity of arousal neurons. From Anatomography, website maintained by Life Science Databases(LSDB). Neural Control of Slow - Wave Sleep The sleep/waking flip -flop ➢ The flip -flop is on when the sleep -promoting neurons in the vlPOA are inhibited and the arousal neurons are active ➢ The flip -flop is off when the sleep -promoting neurons in the vlPOA are activated and the arousal neurons are inhibited Neural Control of Slow - Wave Sleep • Orexinergic neurons help to stabilise the sleep/waking flip/flop • Motivation to remain awake or events that disturb sleep activate the orexinergic neurons. Neural Control of Slow - Wave Sleep • What factors control the activity of the orexinergic neurons? • Biological clock • Hunger related signals activate them • Satiety related signals inhibit them • Orexinergic neurons receiving inhibitory input from the vlPOA because of a build -up of adenosine. Neural Control of Slow - Wave Sleep • Acetylcholinergic neurons also fire at a high rate in REM sleep • There is a REM flip -flop • REM -ON neurons are located in the pons • REM -OFF neurons are located in the midbrain Neural Control of REM Sleep • During waking, the REM -OFF region receives excitatory input from the orexinergic neurons of the lateral hypothalamus, and this activation tips the REM flip -flop into the OFF state. • When the sleep/waking flip -flop switches into the sleep phase, slow -wave sleep begins. • The activity of the excitatory orexinergic , noradrenergic, and serotonergic inputs to the REM -OFF region begins to decrease. As a consequence, the excitatory input to the REM -OFF region is removed. Neural Control of REM Sleep • The REM flip -flop tips to the ON state, and REM sleep begins. • Orexin is very important – it keeps the REM flip -flop in the OFF position Neural Control of REM Sleep • There are also specific neurons that control the muscular paralysis that occurs during REM sleep. • When the REM flip -flop tips to the ON state, motor neurons in the spinal cord become inhibited, and cannot respond to the signals arising from the motor cortex in the course of a dream. • Damage to the “paralysis neurons” removes this inhibition, and the person acts out his or her dreams. • https://www.youtube.com/watch?v=Js50Orx94i M Neural Control of REM Sleep Break… Lecture outline • What is sleep? – Measuring physiological responses associated with wakefulness and sleep – Stages of sleep & EEG activity • Neural basis of arousal and sleep BREAK • Dreams, nightmares and lucid dreaming • Why do we sleep? • Disorders of sleep Dreams • Occur every night – whether we remember them or not! • Little evidence that dreaming has an adaptive function • Revonsuo (2000) suggested that they represent threat -stimulation • Evidence that the particular pattern of brain activity during a dream, represents areas that would be active if the events were occurring Nightmares • Typically defined as a vivid and frightening dream that awakens the dreamer (although there is still some debate; Sandman et al., 2013) • Idiopathic and post -traumatic nightmares • 2 -5% of the population experience frequent nightmares • Aetiology is still unclear but greater experience associated with PTSD, depression, insomnia, and being female Lucid Dreaming • Awareness that you are dreaming while the dream continues • Lucid dreaming can be trained (see video) • Lucid dreaming can also be induced. – Voss and colleagues (2014) induced lucid dreams by applying fronto -temporal transcranial alternating current stimulation ( tACS ). Lucid dreaming induced at two frequencies – 25 and 40Hz • So, lucid dreaming is associated with lower gamma frequency in the fronto -temporal area of the brain • https://www.youtube.com/watch?v=qH -MGqokk_Y Lecture outline • What is sleep? – Measuring physiological responses associated with wakefulness and sleep – Stages of sleep & EEG activity • Neural basis of arousal and sleep BREAK • Dreams, nightmares and lucid dreaming • Why do we sleep? • Disorders of sleep Why Do We Sleep? Functions of Slow - Wave Sleep • Most researchers believe slow -wave sleep allows the brain to rest. • All mammals sleep, some with only one hemisphere at a time if necessary • Slow -wave sleep deprivation affects cognitive abilities, especially sustained attention, but not physical abilities Sleeping with only one hemisphere Sleep in a Dolphin. The two hemispheres sleep independently, presumably so that the animal remains behaviorally alert . Adapted from Mukhametov , L. M., in Sleep Mechanisms , edited by A. A. Borbély and J. L. Valatx . Munich: Springer -Verlag , 1984. Why Do We Sleep? Functions of Slow - Wave Sleep • Cerebral metabolic rate and blood flow falls by about 75%. • This coupled with people’s unresponsiveness, and confusion if awakened suggests cerebral cortex ‘shuts down’ during sleep. • Obviously does give us rest BUT the amount we sleep is not related to amount of exercise we have done that day. Why Do We Sleep? Functions of REM Sleep • If deprived of REM sleep, you will have more REM sleep in the next sleep period (Rebound phenomenon). • Highest proportion of REM sleep occurs during brain development. • Why do adults have REM sleep if it seems to serve such an important function for brain development? • We continue to learn throughout life and both REM sleep and SWS facilitate learning as we will see. • BUT it is possible to function normally with no REM sleep, with no obvious side effects, as shown by people on antidepressants or with brain damage that reduces or eliminates REM sleep. Why Do We Sleep? Functions of REM Sleep Siegel, J. M. (2011). REM sleep: a biological and psychological paradox. Sleep medicine reviews ,15 (3), 139 -142. Why Do We Sleep? Sleep and Learning • Sleep is probably important for the consolidation of memories • Slow -wave sleep and REM sleep appear to play different roles • Two very broad types of memory – Declarative (Explicit) – Nondeclarative (Implicit) Why Do We Sleep? Sleep and Learning Mednick , Nakayama, & Stickgold (2003) • Participants learned a nondeclarative (implicit) visual discrimination task at 9am. • Some participants took a 90min nap during the day • Used EEG to see which participants engaged in REM sleep and which participants did not. • Participants performed the task again at 7pm that night Why Do We Sleep? Sleep and Learning – Mednick et al. results REM Sleep and Learning. The graph shows the role of REM sleep in learning a nondeclarative visual discrimination task. Only after a 90 -minute nap that included both slow -wave sleep and REM sleep did the subjects’ performance improve. Adapted from Mednick , S., Nakayama, K., and Stickgold , R. Nature Neuroscience , 2003, 6, 697 –698. Why Do We Sleep? Sleep and Learning Tucker et al. (2006) • Trained participants on a nondeclarative and a declarative task • Some participants had a one hour nap • But were awakened before they engaged in REM sleep • So those who napped, engaged in slow -wave sleep only Nondeclarative Declarative Pear - Boat Rug - Castle Lemon - Ocean Why Do We Sleep? Sleep and Learning – Tucker et al. Nondeclarative Slow -Wave Sleep and Learning. Subjects learned a declarative learning task (list of paired words) and a nondeclarative learning task (mirror tracing). After a nap that included just slow -wave sleep, only subjects who learned the declarative learni ng task showed improved performance, compared with subjects who stayed awake. Adapted from Tucker, M. A., Hirota , Y., W amsley , E. J., Lau, H., Chaklader , A., and Fishbein , W. Neurobiology of Learning and Memory , 2006, 86 , 241 – 247. Declarative Pear -Boat Rug -Castle Lemon -Ocean Why Do We Sleep? Sleep and Learning • These findings suggest: ➢ REM sleep facilitates consolidation of nondeclarative memories ➢ Slow -wave sleep facilitates consolidation of declarative memories Why Do We Sleep? Sleep and Learning • Studies by Peigneaux et al. (2004) and Wamsley et al. (2010) investigated the role of slow -wave sleep in navigation (learning your way around a virtual town) • Both studies confirmed a role of slow -wave sleep in learning our way around. • We appear to rehearse the information during slow -wave sleep and consolidate learning. Why Do We Sleep? Sleep and Learning • BUT there is still significant debate as to whether both slow -wave sleep and REM sleep are necessary for memory and learning. • Case of 33 year -old who has had very little REM sleep since a brain injury at age 20. Yet, he appears to be able to learn – completed law school and practices as a lawyer. Lecture outline • What is sleep? – Measuring physiological responses associated with wakefulness and sleep – Stages of sleep & EEG activity • Neural basis of arousal and sleep BREAK • Dreams, nightmares and lucid dreaming • Why do we sleep? • Disorders of sleep Disorders of Sleep • Insomnia • Sleep Apnea • Narcolepsy • REM sleep behaviour disorder • Slow -wave sleep problems • Fatal familial insomnia Insomnia • DSM -V criteria – difficulty getting to sleep, staying asleep, or having non -restorative sleep – together with associated impairment of daytime functioning. – Defined in relation to a person’s particular need for sleep. • Chronic insomnia effects approximately 9% of the population while up to 1/3 report at least one nocturnal symptom (Morin & Jarrin, 2013; Singareddy et al., 2012). Causes of Insomnia • Age – More common in older people • Environmental factors – Electronic devices, noise, light – detrimental – White noise or other repetitive noise - beneficial • Physiology – Heightened activity in the reticular activating system • Circadian rhythms – Changes, e.g. through time zone, shift -work patterns • Medical conditions and medications – E.g. Heart and respiratory conditions, some antidepressants, epilepsy medications Taylor, D., Gehrman, P., Dautovich, N. D., Lichstein, K. L., & McCrae, C. S. (2014). Causes of insomnia. In Handbook of Insomnia (pp. 11 -27). Springer Healthcare Ltd. Insomnia Treatment • Typically treated with drugs but can potentially also be treated with mindfulness and CBT (Manber et al., 2011; Ong et al., 2014) • Chronic sleep deprivation can lead to serious health problems – E.g. obesity, diabetes and cardiovascular disease (Orzel -Gryglewska, 2010) Sleep Apnea • Form of insomnia – the inability to sleep and breathe at the same time • Build of carbon dioxide • Carbon dioxide in the blood stimulates chemoreceptors • Disrupts sleep affecting daytime functioning • If caused by obstruction can be corrected surgically or relieved by pressurised air that keeps the airway open Narcolepsy • Symptoms • Sleep attack – overwhelming urge to sleep • Cataplexy – muscular paralysis of REM sleep while awake ➢ Varying degrees of muscle weakness ➢ Can become completely paralyzed while conscious ➢ Generally occurs when the person feels strong emotions or by sudden physical effort. Narcolepsy • Symptoms • Sleep paralysis • REM muscular paralysis just before the onset of sleep or upon waking • Hypnagogic hallucinations • dreaming while awake and paralysed • can very realistic and terrifying. Narcolepsy Cataplexy attack in a dog Dogs - https://www.youtube.com/watch?v=jTj3a2nHw8k Human -https://www.youtube.com/watch?v=d41BfD21b48 Narcolepsy • Causes – Hereditary element – Environmental factors play a role but are unknown – Orexinergic neurons are attacked by the immune system, usually in adolescence (Fontana et al., 2010) Narcolepsy • Treatments – Sleep attacks can be diminished with stimulants such as methylphenidate (Ritalin) – REM sleep phenomenon (cataplexy, sleep paralysis and hypagogic hallucinations) traditionally treated with antidepressant drugs – Most common current treatments are modafanil and/or sodium oxybate (GHB; gamma hydroxybutyric acid), both stimulant drugs REM Sleep Behaviour Disorder • Failure to exhibit paralysis during REM sleep • Acting out dreams • Neurodegenerative disorder with a genetic component (Schneck et al., 1993) • Associated with other neurodegenerative conditions such as Parkinson’s disease (Boeve et al., 2007) • Usually treated with clonazepam, a benzodiazepine tranquilizer (Aurora et al., 2010; Frenette, 2010) • https://www.youtube.com/watch?v=rFXYRQ9xPUA Slow - Wave Sleep Problems • Sleepwalking (Somnambulism) ➢ Not acting out a dream but the person can engage in complex behaviours ➢ More common in children ➢ Genetic component ➢ Disorder of arousal ➢ Sleepwalking facts - https://www.youtube.com/watch?v=bsL7u8qosTM • Night terrors ( pavor nocturnus ) ➢ Anguished screams, trembling, a rapid pulse, and usually no memory of what caused the terror ➢ Hereditary element ➢ https://www.youtube.com/watch?v=4Vh56g9b92U • Bedwetting (nocturnal enuresis) ➢ About 10% of 7 year olds ➢ Heredity element All of these behaviours occur during slow -wave sleep Slow - Wave Sleep Problems Fatal Familial Insomnia • Neurodegenerative condition • Prion disease • Damage to the thalamus • Initially presents with insomnia and very vivid dreams when the person finally manages to sleep. • Psychiatric complications – panic attacks, cognitive deficits, paranoia and phobias • As the disease progresses it affects the autonomic nervous system (e.g. elevated blood pressure) and coordination (ataxia) • EEG shows disturbances and reductions in sleep spindles and K complexes • Disappearance of slow -wave sleep and only brief periods of REM sleep • Ultimately inability to voluntarily move or speak (akinetic mutism), coma, and death. Fatal Familial Insomnia Sleep Disorders Summary • Insomnia – definition, causes, treatment • Sleep apnea – carbon dioxide build -up • Narcolepsy – symptoms, causes and treatment • REM sleep behaviour disorder – acting out dreams • Slow -wave sleep problems – sleep walking, night terrors, bedwetting • Fatal familial insomnia - prion disease, initially presents as insomnia, disappearance of slow -wave sleep Summary • Stages of sleep – Stage 1, Stage 2, slow -wave sleep (stages 3 & 4), REM sleep. • Different patterns of brain activity in each stage • Neural control of arousal, slow -wave sleep and REM sleep • Dreams, nightmares, and lucid dreaming • Function of sleep – rest and consolidate learning Reading • Carlson • Introduction and stages • Neural control of sleep (Physiological mechanisms of sleep and waking) • Why do we sleep Disorders of sleep Optional • https://www.nytimes.com/2001/05/06/magazine/3 - case -study -fatal -familial -insomnia -location -venice - italy -to -sleep -no -more.html References Kolb, B. & Whishaw , I. Q. (2004). Why do we sleep and dream? In An Introduction to Brain and Behaviour. Worth Publishers: New York Revonsuo , A. (2000). The reinterpretation of dreams: An evolutionary hypothesis of the function of dreaming. Behavioral and Brain Sciences, 23(06), 877 -901. Sandman, N., Valli , K., Kronholm , E., Ollila , H. M., Revonsuo , A., Laatikainen , T., & Paunio , T. (2013). Nightmares: Prevalence among the Finnish general adult population and war veterans during 1972 -2007. Sleep, 36(7), 1041 -1050. Stickgold , R., & Walker, M. P. (2013). Sleep -dependent memory triage: evolving generalization through selective processing. Nature Neuroscience, 16, 139 -145. Voss, U., Holzmann , R., Hobson, A., Paulus, W., Koppehele -Gossel , J., Klimke , A., & Nitsche , M. A. (2014). Induction of self awareness in dreams through frontal low current stimulation of gamma activity. Nature neuroscience, 17(6), 810 -812.