Ch9 - Sleep & Biological Rhythms

Question 1

EEG when awake

Answer 1

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

Question 2

Sleep stages

Answer 2

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)

Question 3

Sleep spindles & K complexes

Answer 3

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?

Question 4

REM physiology

Answer 4

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?

Question 5

SWS physiology

Answer 5

Possible dreamlike imagery ← regional cerebral blood flow generally decreased BUT localised increases in visual & auditory cortexes
Decreased blood flow to thalamus & cer`ebellum

Question 6

Why do we sleep?

Answer 6

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)

Question 7

Fatal familial insomnia

Answer 7

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

Question 8

Glymphatic system

Answer 8

Sleep enhances removal of other neurotoxins from brain through glymphatic system - connections between interstitial fluid surrounding cells and CSF

Question 9

Adenosine

Answer 9

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

Question 10

Neurotransmitters & arousal

Answer 10

Acetylcholine (memory), norepinephrine (vigilance), serotonin (behavior), histamine (wakefulness, arousal), orexn

Question 11

Acetylcholine

Answer 11

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

Question 12

Norepinephrine

Answer 12

Noradrenergic system of the locus coeruleus in dorsal pons

Question 13

Serotonin 5-HT

Answer 13

Raphe nuclei in medullary & pontine regions of reticula project to many areas which correlate with waking (decreasing in SWS, 0 in REM)

Question 14

Histamine

Answer 14

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

Question 15

Orexin

Answer 15

(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

Question 16

Preoptic area

Answer 16

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

Question 17

Neural control of transition to REM

Answer 17

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

Question 18

Insomnia pharmacological treatments

Answer 18

zolpidem (Ambien) or zaleplon (Sonata) - hypnotics; agonists at GABA - also benzo & over-the-counter antihistamines

Question 19

Sleep apnea

Answer 19

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

Question 20

Narcolepsy

Answer 20

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

Question 21

Narcolepsy cause

Answer 21

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

Question 22

Narcolepsy treatment

Answer 22

Treated w stimulants like methylphenidate (catecholamine agonist) or modafinil - REM phenomena alleviated by antidepressants-facilitates serotonergic & noradrenergic activity

Question 23

Problems with SWS

Answer 23

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

Question 24

Retinohypothalamic pathway

Answer 24

Direct projection retina → Suprachiasmatic nucleus SCN

retinohypothalamic pathway - special photoreceptor - photochemical melanopsin (present in ganglion cells, sensitive)

Question 25

Biological clock pathway

Answer 25

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

Question 26

Time units

Answer 26

protein production levels & degradation (negative feedback loop)

chromosome 2? (mutation → advanced sleep phase syndrome; 4 hour advance

Question 27

seasonal rhythms

Answer 27

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