Ch9 - Sleep & Biological Rhythms Flashcards
EEG when awake
Alpha - regular, medium-f 8-12Hz (cycles per second)
Resting quietly, more prevalent when eyes closed
Beta - irregular, mostly low-amplitude 11-30Hz or 13-20Hz
Desynchrony (many diff neural circuits actively processing info)
Alert, paying attention, thinking actively
Sleep stages
Stage 1: theta 3.5-7.5 - firing in neurons of neocortex is becoming more synchronised - Hypnic jerks, falling sensation
Stage 2 (after 10 minutes): irregular, theta activity. Sleep spindles & K complexes
SWS - Stage 3 & 4 (only diff is how much delta activity): delta, slow-wave 4Hz high amplitude
REM, theta & beta - paralysis due to restriction to our spinal & cranial motor neurons (not eye movement & respiration)
Sleep spindles & K complexes
Sleep spindles (occurring 2-5 times in stages 1-3) play a role in staying asleep in response to external stimuli, correlated with intelligence K complexes, 1 per minute, triggered by unexpected noises, role in bringing into deeper sleep?
REM physiology
Rate of cerebral blood flow is high in extrastriate cortex (visual association) but low in striate (not receiving input) & prefrontal cortex (dreams make no sense)
Lucid dreams = activation of the prefrontal cortex?
SWS physiology
Possible dreamlike imagery ← regional cerebral blood flow generally decreased BUT localised increases in visual & auditory cortexes
Decreased blood flow to thalamus & cer`ebellum
Why do we sleep?
Rest from slow wave sleep & learning & brain development from REM
Reduced metabolic rates permit restorative mechanisms in cells to destroy free rascals & prevent their damaging effects (slow wave)
Fatal familial insomnia
inherited neurological disorder resulting in damage to portions of thalamus - deficits in attention & memory, dreamlike, confused state, loss of control to autonomic nervous system & endocrine system, increased body temp, insomnia
Reductions in sleep spindles & K-complexes
Slow wave sleep disappears, only brief episodes of REM remain
Glymphatic system
Sleep enhances removal of other neurotoxins from brain through glymphatic system - connections between interstitial fluid surrounding cells and CSF
Adenosine
Adenosine increases in wakefulness & glycogen (produced by astrocytes) is converted to fuel- during SWS, neurons in brain rest (by adenosine which inhibits activity (which is deactivated by coffee)) & astrocytes renew stock of glycogen
People with G/A allele for gene that encodes for enzyme adenosine deaminase (breaks down adenosine) spend 30 mins more time in slow wave sleep
Neurotransmitters & arousal
Acetylcholine (memory), norepinephrine (vigilance), serotonin (behavior), histamine (wakefulness, arousal), orexn
Acetylcholine
2 groups: pons & forebrain - produce activation & cortical desynchrony when stimulated
3rd group in medial septum - controls hippocampus activity
Agonists increase EEG sights of cortical arousal
High levels ACh in hippocampus & neocortex (alertness) during waking & REM, low during slow-wave sleep
Norepinephrine
Noradrenergic system of the locus coeruleus in dorsal pons
Serotonin 5-HT
Raphe nuclei in medullary & pontine regions of reticula project to many areas which correlate with waking (decreasing in SWS, 0 in REM)
Histamine
Tuberomammillary nucleus (TMN) of hypothalamus project to a bunch - directly to cerebral cortex, increasing cortical activation & arousal - indirectly to forebrain & dorsal pons, increasing release of ACh in cerebral cortex - low during slow wave & rREM
Orexin
(peptide) containing cell bodies in lateral hypothalamus project to tons of areas with excitatory effect - high when awake and highest with exploratory activity (rats)
Blue light w optogenetic activation of these neurons
Narcolepsy treated w modaflin - stimulates release of orexin in TMN, which activates histamine there
Preoptic area
Controls a region of anterior hypothalamus (most involved in initiation of sleep)
When active, suppresses activity of arousal neurons → fall asleep
Most located in ventrolateral preoptic area (vIPOA) - some in median preoptic nucleus (MnPN, where damage suppresses sleep, activity increases during sleep) - secrete GABA
Reciprocal inhibition - flip flop
Neural control of transition to REM
Flip-flop SWS vs REM - noradrenergic & seretoneric gradually decrease as we sleep → more excitatory input to REM-OFF removed → ON → ACh activated
REM-ON neurons in sublaterodorsal nucleus in dorsal pons - eye mov & genital activity
REM-OFF in ventrolateral periaqueductal grey matter (vIPAC)
Interconnected by inhibitory GABAergic neurons
Insomnia pharmacological treatments
zolpidem (Ambien) or zaleplon (Sonata) - hypnotics; agonists at GABA - also benzo & over-the-counter antihistamines
Sleep apnea
stop breathing when asleep - CO2 in blood stimulates chemoreceptors, person wakes up gasping for air cycle - most can be corrected by mechanically keeping airways open
Narcolepsy
Changes in orexin system resulting in sleep at inappropriate times
Sleep attaches: 2-5 minutes, wakes up feeling refreshed
Cataplexy: varying amounts of muscle weakness/conscious paralysis = REM - strong emotional reactions or sudden physical effort
Sleep paralysis - inability to move just before onset of sleep or waking in morning - hypnagogic hallucinations dreams paralysed awake
Narcolepsy cause
1/ in 2000 ppl, chromosome 6 - product of gene (in dogs) is a receptor for orexin. In humans, caused by hereditary autoimmune disorder attacking orexinergic neurons
Narcolepsy treatment
Treated w stimulants like methylphenidate (catecholamine agonist) or modafinil - REM phenomena alleviated by antidepressants-facilitates serotonergic & noradrenergic activity
Problems with SWS
Bedwetting (nocturnal enuresis), sleepwalking (somnambulism), night terrors (pavor nocturnus) - all most frequent in children - heritable sleep-related eating disorder treated with dopaminergic agonists or topiramate (antiseizure), may be provoked by zolpidem
Retinohypothalamic pathway
Direct projection retina → Suprachiasmatic nucleus SCN
retinohypothalamic pathway - special photoreceptor - photochemical melanopsin (present in ganglion cells, sensitive)
Biological clock pathway
SCN (efferent) → subparaventricular zone (SPZ, dorsal to SCN) → dorsomedial nucleus of hypothalamus → several brain lesions, sleep & waking (viPOA, inhibit sleep & orexinergic, promote)
SCN can also control rhythms by chemical signal prokineticin 2 (protein in SCN neurons) diffusion through extracellular fluid
Time units
protein production levels & degradation (negative feedback loop)
chromosome 2? (mutation → advanced sleep phase syndrome; 4 hour advance
seasonal rhythms
Pineal gland (on top of midbrain, in front of cerebellum) secretes melatonin at night → controls hormones, physiological processes, & behavior - hibernation
Neurons in SCE make indirect connections with neurons in paraventricular nucleus of hypothalamus (PVN) → spinal cord, form synapses with preganglionic neurons of sympathetic nervous system - postganglionic innervate & controls secretion of melatonin
Melatonin can affect sensitivity of SCN neurons to zeitgebers & cn itself alter circadian rhythms
