Ch9: Sleep and Biological Rhythms

Question 1

What is Electroencephalogram (EEG) used for and what levels of activity does it show?

Answer 1

Electrodes are attached to sleeper’s scalp to study sleep by monitoring the brain’s activity
-> shows alpha: smooth electrical activity of 8-12Hz associated with a state of relaxation (sometimes occur when person’s eyes are open but more prevalent when closed)
-> shows beta activity: irregular electrical activity of 13-30Hz associated with a state of arousal (shows desynchrony which reflects the fact that many different neural circuits in the brain are actively processing info => occurs when person is alert and paying attention to event sin the environment or is thinking actively) (shows as chaotic waveforms without clear pattern)

other electrodes and transducing devices can be used to monitor autonomic measures such as heart rate, respiration, and changes in the ability of the skin to conduct electricity

Question 2

What device is used to record electrical potential from an electrode placed on or in a muscle?
What does it monitor?

Answer 2

Electromyogram (EMG): placed on face to monitor muscle activity

Question 3

What device is used to record electrical potential from the eyes?
Where are electrons placed and what does it detect?

Answer 3

Electro-Oculogram (EOG):
-> placed on skin around eyes
-> detects (rapid) eye movements

Question 4

What is the difference between the original stages of sleep and the new ones?

Answer 4

Stage 4 of sleep doesn’t exist anymore, stage 3 and 4 were combined -> slow-wave sleep
=> there are now 3 stages of non-REM sleep and then the REM sleep stage
AND the difference of the old way of viewing sleep was on how much delta activity was observed

Question 5

What’s before the first stage of sleep and what is its activity?

Answer 5

Awake
-> Alpha activity: smooth 8-12Hz (relaxed)
-> Beta Activity: irregular 13-20Hz (aroused) (irregularity due to neurons firing as needed to do what you’re doing like listening to music)

Question 6

What stage of sleep is theta activity in, at what frequency and what does it indicate? When does Theta activity occur?

Answer 6

Stage 1 at 3.5-7.5Hz indicating that firing of neurons in the neocortex is becoming more synchronized and occurs intermittently during early stages of SWS and REM sleep

Question 7

Which stage is a transition between sleep and wakefulness?

Answer 7

Stage 1

Question 8

What happens during stage 1 sleep and how long does it last?

Answer 8

Waves get slower due to the slowing of brain activity which starts to develop a synchrony
Doesn’t last long maybe 10 minutes and then we enter stage 2

Question 9

Are sleep stages categorical or a spectrum?

Answer 9

Spectrum: not stepping down from one stage to the next

Question 10

What activity is present in stage 2 sleep? Frequency and times of reaccurence?

(2 activities)

Answer 10

Sleep Spindle: short bursts of 12-14Hz that occur between 2 and 5x a minute during stages 1 to 3
K complex: sudden sharp waveforms which happen only during stage 2 sleep

Question 11

Role of stage 2 sleep?

Answer 11

Keeps individuals asleep especially in response to external stimuli like sounds
Consolidation of memory

Question 12

In which stage does consolidatin of memory occur and why?

Answer 12

Due to the presence of K complex waveforms, there is consolidation of memories

Question 13

What happens if a person is woken up during stage 2 of sleep?

Answer 13

They might report that they haven’t been asleep

Question 14

How long does stage 2 sleep last?

Answer 14

15 minutes

Question 15

What activity can be found in stage 3-4 of sleep? Frequency? Name of this stage and reason for it?

Answer 15

Delta activity: regular, synchronous activity less than 4Hz (20-50%) which signals slow-wave sleep
-> occurs during deepest stage of SWS
Brain is slowing down, not really activating

Question 16

Why is synchrony important in SWS?

Answer 16

indicates that we’re in SWS stage

Question 17

Which stage is deepest stage of sleep? What happens if you wake person up from that stage? frequency of delta activity at this stage?

Answer 17

SWS: only loud noises will wake a person in this stage
stage 4: 50% delta activity
When awakened from this stage: acts groggy and confused and if asked if they were dreaming, will most likely say no but if questioned more carefully, they might report a thought, image or some emotion

Question 18

What is another name for REM sleep and why?

Answer 18

Paradoxical sleep bcs the person is asleep but doesn’t appear like it bcs of rapid eye movements, rapid eye movements, brain activy become rapid and irregular so it looks like they’re activating their brain (desynchrony)

Question 19

In what stage do we dream and muscular paralysis occurs? Why is muscle paralysis important

Answer 19

REM/Paradoxical sleep
muscle paralysis important bcs you could act out your dreams otherwise => it inhibits spinal and cranial motor neurons but not neurons that control respiration and eye movement and brain is still very active

Question 20

What happens after 90 minutes after beginning of sleep?

Answer 20

Abrupt change in some of the physiological measures recorded

Question 21

What types of waves could we find occasinoally in REM sleep?

Answer 21

Theta waves at same frequency as stage 1 and beta activity as well

Question 22

Examples of physiological activity in REM sleep?

Answer 22

-> eyes dart about rapidly
-> acceleration and decelration of heart rate
-> irregular breathing
-> increased brain activity
-> penile erection or vaginal secretion: in REM sleep cerebral blood flow and oxygen consumption are accelerated

Question 23

Are people in REM easily awakened and aroused?

Answer 23

Yes, during REM sleep a person might not react to most noises, but they are easily aroused by meaningful stimuli like name (e.g.)

Question 24

What happens when awakened from sleeping? What is a particularity about REM sleep dreams?

Answer 24

Person is alert and attentive and will likely report they were dreaming which tend to be of a narrative form with a storyline and progression of events

Question 25

How do stages work during the night? Alternate? How long is each cycle?

Answer 25

People alternate between periods of REM and non-REM sleep
each cycle is approx. 90 minutes long (20-30 minute of REM sleep

8 hour sleep will contain typically 4-5 periods of REM sleep

Question 26

Which waves are synchronous/desynchronous and in what stage can they be found?

Answer 26

synchronous:
-> alpha activity (8-12Hz): waking stage
-> delta activity (<4Hz): woekfjw
desynchronous:
-> theta activity (3.5-7.5Hz): stage 1+REM
-> beta activity (13-20Hz): waking+REM

hehe trick qs suckaaaaa

Question 27

In what stages do similar patterns of EEG activity occur?

Answer 27

stage 1 and REM: theta activity

Question 28

When does most of SWS sleep occur and what happens to REM duration?

Answer 28

most SWS sleep occurs during 1st half of the night and contain more and more stage 2 sleep whereas priods of REM sleep become longer throughout the night

Question 29

What difference is there between adult sleep cycle’s and baby’s?

Answer 29

babies differ in what they enter: they spend more time in REM sleep earlier on than adults and REM is more important for children because they are still learning -> consolidation of memory
-> highest proportion of REM sleep is seeing during the most active phase of brain development in infancy and childhood
-> more important bcs REM sleep consolidates for nondeclarative memory (implicit memory) and all babies learn is learning how to move, control their heads, crawl -> non-declerative activities

Question 30

are we unconscious when we sleep?

Answer 30

No, we just don’t respond to the environment

Question 31

How are the Prefrontal, extrastriate and striate cortex involved in REM?

Answer 31

Prefrontal cortex:
-> low activity during REM
-> reflects lack of organization and planning that occur in dreams seeing as it is involved in organizing events in time and disntiguishin illusion from reality => low activity so non of that
-> e.g.: in dreams, past, present and future are interchanged or timing of events is unrealistic

Extrastriate cortex (visual association cortex):
-> high acivity during REM
-> reflects visual hallucinations during dreaming

Striate cortex:
-> low activity in REM due to lack of visual input: makes sense cuz eyes closed so aren’t receiving any visual input cuz usually 1st step of visual info but since you’re not seeing aything then it doesn’t need to be activated
-> low rate of cerebral blood flow during REM sleep

Question 32

what phenomenon happens during REM caused by the activation of the prefrontal cortex?

Answer 32

lucid dreaming: awareness that you’re dreaming but aren’t awake

Question 33

Can dreaming occur in SWS?

Answer 33

not really but changes in brain activity can accompany dreamlike imagery experienced during SWS
usually no though cuz: regional cerebral blood flow during SWS is generally decreased throuhgout the brain compared to waking and blood flow to the thalamus and cerebellum is decreased as well

Question 34

Why do we sleep? Functions of sleep

What is the primary function of SWS?

Answer 34

permit the brain to rest and recover from its daily cognitive activity
not needed for normal body function -> more important for brain to rest than body

sleep isn’t for the body although it does help the body through the period of not moving which is what body needs to rest but sleep’s goal isn’t to let body rest

Question 35

Why do we sleep? Functions of sleep

Is sleep the most insistent drive?

Answer 35

after effects of severe pain and the need to breathe

people can commit suicide by refusing the need to drink but not even the most determined person can defy the urge to sleep indefinitely -> it’ll come sooner or later

Question 36

Why do we sleep? Functions of sleep

What do REM and SWS sleep promote, respectively?

Answer 36

REM: learning and brain development
SWS: learning

Question 37

Why do we sleep? Functions of sleep

Is sleep a universal phenomenon?

Answer 37

Among vertebrates + is essential for survival

Question 38

Why do we sleep? Functions of sleep

In what stages of sleep is mental activity present?

Answer 38

both REM and SWS

Question 39

Why do we sleep? Functions of sleep

Can someone die from lack of sleep?

however…

Answer 39

not unless it’s forced on person bcs of abuse or diseases (e.g., fatal insomnia) => only if you’re specifically prevented from sleeping can it be fatal
=> we are able to survive and function (reasonably well) despite occasional loss of sleep
=>BUT could be detrimental to cognitive abilities (especialy on tasks that require attention or vigilance):
-> could be caused even by one night of sleep deprivation and extended sleep loss amplifies these effects
-> lose ability to comprehend, rationally think, etc
-> cognitive abilities are 1st to go

=>adverse health outcomes caused by regular or extensive sleep deprivation:
->weight gain, obesity, diabetes, hypertension, heart disease, stroke, depression, impaired immune function, increased pain, greater risk of accidents, increased risk of death

Question 40

Why do we sleep? Functions of sleep

Can someone recover from sleep deprivation?

Answer 40

A lot of the hours lost are never made up but the majority of the sleep that is made-up for is SWS and REM sleep => priority over stage 1-2 of sleep (NREM sleep)

Question 41

Why do we sleep? Functions of sleep

What’s unique about dolphin sleeping cycle?

Answer 41

Sleep a hemisphere at a time to keep themselves alive => they can keep swimming and swim up to breath

Question 42

Why do we sleep? Functions of sleep

Functions of SWS

Answer 42

-> primary function: permit brain to rest (essential for survival)
-> decrease glucose metabolism in frontal lobes which is high during the day due to tasks that demand alertness and mental activity
-> reduces free radicals: brain waste = highly oxidizing agents that can bind with electrons from other molecules and damage the cells in which they are found, process known as oxidative stress

Question 43

Why do we sleep? Functions of sleep

When does SWS increase?

Answer 43

after a day of rigorous mental activity or several weeks of working memory training

Question 44

Why do we sleep? Functions of sleep

How are free radicals created and how are they eliminated?

Answer 44

As our brain works (thinking, writing, etc), it produces waste from conversion of ATP and this accumulation can cause problems which is why it needs to be reduced and SWS is where this happens

Question 45

Why do we sleep? Functions of sleep

Why is SWS important?

free radicals (brain waste)

Answer 45

Prolonged sleep deprivation, preventing someone from SWS repeatedly for a long period of time means free radicals =increased in radicals -> not being reduced = oxidativestress
-> could be fatal

Question 46

Why do we sleep? Functions of sleep

Name and explain a hereditary disorder characterized by progressive insomnia

Answer 46

fatal familia insomnia
-> related to Creutzfeldt-Jacob disease and madcow disease
-> results in damage to portions of the thalamus
-> starts in adulthood
-> don’t know if insomnia causes symptoms or symptoms cause insomnia

Question 47

Why do we sleep? Functions of sleep

What are the symptoms of fatal familia insomnia?

Answer 47

-> deficits in attention and memory followed by dreamlike, confused state
-> loss of control of ANS and endocrine system
-> increased body temperature
-> insomnia
-> death (usually within 12 months

Question 48

Why do we sleep? Functions of sleep

What are the 1st signs of sleep disturbance in fatal familia insomnia?

Answer 48

reductions in sleep spindles and K complexes
-> as disease progresses, SWS completely disappears and only brief episodes of REM sleep remain

certain drugs can help patient sleep and could give them higher quality of life as well as maybe extending the life exptancy but still fatal

Question 49

Why do we sleep? Functions of sleep

Functions of REM sleep?

Answer 49

-> promote brain development
-> time of intense physiological activity
-> rapid eye movement, accelerations and decelerations and in heart rate, irregular breathing, increase in brain activity
-> facilitates learning

Question 50

Why do we sleep? Functions of sleep

Can you live without REM?

Answer 50

yes but not SWS
-> BUT might not learn or hold as much memory consolidation

Question 51

Why do we sleep? Functions of sleep

What happens when woken up from REM vs woken up after REM?

Answer 51

from REM: won’t remember dreaming
not from REM: remember dreaming

Question 52

Why do we sleep? Functions of sleep

What happens with increase of REM sleep deprivation?

Answer 52

REM rebound phenomenon: increased frequency or intensity of REM sleep after temporarily suppressed
-> people have to be waken up more frequently bcs of how deep into REM they are
-> spend more time in REM sleep
-> deficiency is made up when uninterrupted sleep is permitted

Question 53

Why do we sleep? Functions of sleep

What does REM rebound phenomenon suggest?

Answer 53

that REM sleep is controlled by a regulatory system bcs with its deprivation, its duration is increased => there is a need for a certain amount of REM sleep

Question 54

Why do we sleep? Functions of sleep

Children need more REM sleep because their brain is still developing but then why do adults need it?

Answer 54

REM sleep facilitates the massive changes that happen during development but also some of the more modest changes for learning that occur throughout the lifespan

Question 55

Why do we sleep? Functions of sleep

What are the 2 major categories of long-term memories?

Answer 55

declarative memory (explicit memory): the ones that people can talk (or declare) about, such as memories of past episodes in their lives

non-declarative memory (implicit memory): includes memories learned through experience and practice that don’t necessarily involve an attempt to “memorize” info, such as learning to drive a car, throwing and catching a ball, or recognizing a person’s face

Question 56

Why do we sleep? Functions of sleep

Which type of long-term memory includes memories of relationships between stimuli or events, such as spatial relationships between landmarks we use to navigate around our environment

Answer 56

declarative memory (explicit memory)

Question 57

Why do we sleep? Functions of sleep

What does sleep help consolidate? Which stage does what?

Answer 57

long-term memory:
-> declarative (explicit; gained through experience) facilitated by SWS (e.g., catching a ball)
-> non-declarative facilitated by REM

experiments have shown that participants do better on the exerice of the study after nap (SWS) but even better after REM sleep

Question 58

Why do we sleep? Functions of sleep

Learning a list of paired words is an example of what type of task/memory?

Answer 58

declarative task (explicit memory)

Question 59

Why do we sleep? Functions of sleep

Learning to trace a pencil-and-paper design while looking at the paper in the mirror is what type of task/memory?

Answer 59

non-declarative task (implicit memory)

Question 60

Why do we sleep? Functions of sleep

If someone were to nap and be woken up before REM sleep after performing a declarative and a nondeclarative task, which one would they perform better after the nap?

Answer 60

the declarative task bcs they only slept during SWS, so no consolidation for nondeclarative (REM)

sleeping brainm rehearses info that was acquired during the previous period of wakefulness (newly learned info)

Question 61

Physiological mechanisms of sleep and waking

Why is it stated that sleep is regulated?

chemical control of sleep

Answer 61

If an organism is deprived of SWS or REM sleep, the organism will make up at least part of the missed sleep when permitted to do so

Question 62

Physiological mechanisms of sleep and waking

What happens to SWS the night after a nap?

chemical control of sleep

Answer 62

SWS obtained during a daytime nap is deducted from the amount of SWS obtained the next night
=> these facts suggest that some physiological mechanism monitors the amount of sleep that an organism needs to keep track of the sleep debt we incur during hours of wakefulness

Question 63

Physiological mechanisms of sleep and waking

What is accumulated during wakefulness and destroyed during sleep?
What happens to this process the longer you stay awake?
What is a possible substance?

chemical control of sleep

Answer 63

body produces sleep-promoting substance
-> the longer someone is awake, the longer they have to sleep to deactivate the substance
-> adenosine

Question 64

Physiological mechanisms of sleep and waking

What does brain do when sleep is controlled by chemicals in the blood? How does it related to REM?

chemical control of sleep

Answer 64

Hemisphere of the rain incurs its own sleep debt
->REM sleep deprivation produces independent REM sleep debt

Question 65

Physiological mechanisms of sleep and waking

What is adenosine? How does it work (process)?

neural control of sleep

Answer 65

A nucleoside neuromodulator that’s released by neurons engaging in high levels of metabolic activity; may play a primary (major) role in the initiation of sleep
-> accumulates when we’re awake and reduced during SWS
-> In times of increased brain activity, glycogen found in small stock of nutrients contained by astrocytes, is converted into fuel for neurons => prolonged wakefulness decreases level of glycogen in the brain which increases level of extracellular adenosine which inhibits neural activity and serves as sleep-promoting substance
-> During SWS, neurons in the brain rest and astrocytes renew their glycogen stock

Question 66

Physiological mechanisms of sleep and waking

When are cognitive and emotional effects seen durign sleep deprivation caused?

neural control of sleep

Answer 66

when wakefulness is prolonged and more adenosine is accumulated which inhibits neural activity

Question 67

Physiological mechanisms of sleep and waking

If we spend all day watching tv, would that increase or decrease the level of adenosine and why?

neural control of sleep

Answer 67

less cognitive activity means less tired => less adenosine
=> more cognitive activity means higher levels of adenosine

Question 68

Physiological mechanisms of sleep and waking

How does caffeine affect adenosine effects? What happens when effects wear off?

neural control of sleep

Answer 68

caffeine blocks adenosine receptors aka direct antagonist => adenosine being a neuromodulator that acts on its own receptors, by blocking those, caffeine tricks the brain into thinking there’s less adenosine present
When the caffeing wears off, all of the adenosine that was blcoked gets to the neuromodultor in a higher quantity

Question 69

Physiological mechanisms of sleep and waking

What about people that have caffeine before bed and fall asleep no problem?

neural control of sleep

Answer 69

Might have adapted and have more adenosine receptors

to avoid crash once caffeine wears off, you should take caffeine an hour o 2 after you wake up bcs you don’t actually need it right as you wake up, it’s just more of a habit at that point

Question 70

Physiological mechanisms of sleep and waking

How do genetic factors affect the typical duration of a person’s SWS?

neural control of sleep

Answer 70

Variability in the gene that encodes for adenosine deaminase enzyme (breakdown of adenosine) causes a prolonged duration of SWS sleep bcs adenosine is decreaseing slowly due to this G/A gene

Question 71

Physiological mechanisms of sleep and waking

What are the 5 NTs that are involved in arousal?

neural control of arousal

Answer 71

Acetylcholine, Norepinephrine/noradrenaline, serotonin, histamine and orexin

Question 72

Physiological mechanisms of sleep and waking

What is the role of acetylcholine (ACh)?

neural control of arouasl

Answer 72

-> arousal of cerebral crotex
-> ACh neurons in (dorsal) pons and basal forebrain produce activation and cortical desynchrony when stimulated
-> 3rd group of ACh neurons, in medial septum, controls activity of hippocampus
-> active in wakefuleness and REM (periods during which there is desynchonized activity
-> low during SWS
-> brain becomes active in REM bcs of acetylcholine
-> acetylcholinergic antagonists decrease cortical arousal caused by ACh

Question 73

Physiological mechanisms of sleep and waking

Norepinephrine/Noradrenaline role in arousal? When is it activated and deactivated? Where is it found?

neural control of arousal

Answer 73

-> found in locus coeruleus (LC): dark-colored group of NE cell bodies located in (dorsal) pons near rostral end of the 4th ventricle involved in arousal and vigilance
-> give rise to axons that branch wideley and release NE throughout the neocortex, hippocampus, thalamus, cerebral cortex, pons, medulla => affect widespread and important regoins of the brain
-> Noradrenergic systems of LC mediate catecholamine agonists to produce arousal and sleeplessness
-> Firing rate highest during waking, low during SWS and practically at 0 during REM sleep

Question 74

Physiological mechanisms of sleep and waking

Serotonin’s (5-HT) role in arousal? location? time of activation and slowed firing rate?

neural control of arousal

Answer 74

-> Activates behaviour
-> found mostly in raphe nuclei: group of nuclei found in reticular formation of the medulla, pons, and midbrain, situated along the midline
-> axons project to many parts of the brain, including thalamus, hypothalamus, basal gnaglia, hippocampus, and neocortex
-> stimulation of the raphe nuclei causes locomotion and cortical arousal
-> most active during waking, firing rate declines during SWS and becomes virtually 0 during REM sleep and once REM sleep ends, neurons become temporarily very active again

Question 75

Physiological mechanisms of sleep and waking

What drug prevents the synthesis of serotonin => reduces cortical arousal?

neural control of arousal

Answer 75

PCPA

Question 76

Physiological mechanisms of sleep and waking

Role of histamine in arousal? Location? When is its activity high/low?

neural control of arousal

Answer 76

-> supporting role
-> general NT, no specific role, just involved in awakeness
-> compound synthesized from amino acid histidine
-> found in tuberomammillary nucelus (TMN): nucleus in ventral posterior hypothalamus, just rostral to mammillary bodies
-> axons of these neurons project primarily to the cerebral cortex, thalamus, basal ganglia, basal forebrain, other regions of they hypothalamus
-> projections to the cerebral cortex directly increase cortical activation and arousal
-> projection to acetylcholinergic neurons of the basal forbrain and dorsal pons do so indirectly, by increasing the release of of ACh in the cerebral cortex
-> high activity during waking, low during SWS and REM sleep

Question 77

Physiological mechanisms of sleep and waking

What are antihistamines?

neural control of arousal

Answer 77

particular role in arousal: for allergies, block histamine receptors in brain=>you get really tired, sleepy, can cause drowsiness
-> modern antihistamines can’t cross the blood-brain barrier=> don’t cause drowsiness

Question 78

Physiological mechanisms of sleep and waking

What do injections of drugs that prevent the synthesis of histamine cause? Other way around (infusion of histamine in basal forebrain)?

neural control of arousal

Answer 78

-> decrease in waking and increase in sleep
-> increase in waking, decrease in non-REM sleep

Question 79

Physiological mechanisms of sleep and waking

Orexin role in arousal? location? high/low levels when?

neural control of arousal

Answer 79

peptide also known as hypocretin, produced by neurons whose cell bodies are located in the (lateral) hypothalamus
-> destruction of these cells cause narcolepsy
-> excitatory effect on all the arousal regions: locus coeruleus (NE), raphe nuclei (5-HT), tuberomammillary nucleus (Histamine), and pons and basal froebrain (acetylcholinergic neurons)
-> low rate during SWS and REM sleep but high during waking and when alert

Question 80

Physiological mechanisms of sleep and waking

What is narcolepsy? What causes it? How is it treated?

neural control of arousal

Answer 80

treated with modafinil (orexin agonist): drug that suppresses the drowsiness associated with this disorder
-> stimulate release of orexin in TMN, which activates the histaminergi neurons there

Question 81

Physiological mechanisms of sleep and waking

SUMMMARY of chemical control: What are the different levels of arousal neurons and their location? + sleep-promoting neuron?

neural control of arousal

Answer 81

Adenosine: increase with longer periods of wake (waking levels); low levels during SWS and REM sleep
ACh: found in pons, basal forebrain, medial septum (hippocampus); high levels during waking, low levels during SWS and REM sleep
NE: found in locus coeruleus; high levels during waking, low levels during SWS and REM sleep
Serotonin: found in raphe nuclei, high levels during waking, level decreases during SWS and low levels during REM sleep
Histamine: found in tuberomammillary nucleus, high levels during waking, low levels during SWS and REM sleep
Orexin: found in lateral hypothalamus, high levels during waking, low levels during SWS and REM sleep

Question 82

Physiological mechanisms of sleep and waking

What largely controlss the level of brain activity and what would be the difference between high and low levels of these?

neural control of sleep transitions

Answer 82

the 5 sets of arousal neurons control the level of brain activity
-> high levels of these neurons keep us awake
-> low levels of these neurons puts us to sleep

Question 83

Physiological mechanisms of sleep and waking

What are the 3 factors that control sleep?

neural control of sleep transitions

Answer 83

Homeostatic factors: contol of sleep is homeostatic due to adenosine
-> follows the principles that regulate our eating and drinking

The allostatic conscious attempt to control sleep: reactions to stressful events in the enviroment (danger, lack of water, etc) that serve to override homeostatic control
-> mediated by hormonal and neural reponses to stressful situations and by neuropeptides (e.g.: orexin) that are involved in hunger and thirst
-> e.g.: you have a paper due the next day that hasn’t been started => you drink caffeine (adenosine antagonist) and ask your roomate to wake you up if you fall asleep, walk around to stay awake etc. => conscious attempt to hold off homeostatic input with allostatic control

Circadian factors: restrict sleep to a particular portion of the day/night cycle (time of day factors)
-> we tend to get tired at night and we’re awake during the day but it can depend, someo people have night shifts and sleep during the day and are awake at night instead

Question 84

Physiological mechanisms of sleep and waking

Can we hold off the homeostatic control? If yes, how?

neural control of sleep transitions

Answer 84

Yes we have a say in whether or not we “listen” to the homeostatic factor/control
e.g.: I’m tired but I wanna finish studying this chapter

Question 85

Physiological mechanisms of sleep and waking

Why is the allostatic factor an attempt and temporary?

neural control of sleep transitions

Answer 85

It’s temporary bcs eventually we will fall asleep and it’s an attempt bcs it will only work in the short term

Question 86

Physiological mechanisms of sleep and waking

What allostatic input is really good at holding off sleep? Is there a neuron involved?

neural control of sleep transitions

Answer 86

hunger: done with orexin
-> when you don’t eat, orexin increases and main allostatic input will be lost so to stay awake you shouldn’t eat
-> animals: don’t know when they’ll eat next so why go to sleep if you’ll be even more hungry when you wake considering you’re already hungry now

Question 87

Physiological mechanisms of sleep and waking

What controls the arousal neurons?

neural control of sleep transitions

Answer 87

Preoptic area: region of the anterior hypothalamus involved in the initiation of sleep
-> contains neurons whose axons form hinihibotry synapse connections with the brain’s arousal neurons => when preoptic neurons (sleep neurons) become active, they suppress the activity of our arousal neurons and we fall asleep

Question 88

Physiological mechanisms of sleep and waking

What is the group of GABAergic neurons in the preoptic area and what do they do?

neural control of sleep transitions

Answer 88

Ventrolateral preoptic area (vlPOA) whose activity suppresses alertness and behavioral arousal and promotes sleep
-> activity of these neurons, measured by levels of Fos protein, increases during sleep
-> sleep neurons secrete the inhibitory NT GABA and send their axons to the 5 brain regions involved in arousal

Question 89

Physiological mechanisms of sleep and waking

Which area contains the majority of sleep neurons? What would damage to this area cause?

neural control of sleep transitions

Answer 89

ventrolateral preoptic area (vlPOA)
-> damage to this area would suppress sleep

Question 90

Physiological mechanisms of sleep and waking

Which area contains the majority of sleep neurons?

neural control of sleep transitions

Answer 90

ventrolateral preoptic area (vlPOA)

Question 91

Physiological mechanisms of sleep and waking

What’s another area in the preoptic area that contains some sleep neurons

neural control of sleep transitions

Answer 91

median preoptic nucleus

Question 92

Physiological mechanisms of sleep and waking

What is the Sleep/waking flip-flop? Once asleep, does it control our sleep cycle?

neural control of sleep transitions

Answer 92

determines when we wake and when we sleep
-> once we fall asleep the REM flip-flop controls our cycles of REM and SWS

Question 93

Physiological mechanisms of sleep and waking

What is the REM flip-flop? How does it work?

neural control of sleep transitions

hint: neurons from arousal system and sleep-promoting region can’t be active at the same time

Answer 93

Sleep-promoting region in vlPOA can’t be active at the same time as Brain stem and forebrain arousal systems => mutual inhibition
->Both systems are connected by inhibitory GABAergi neurons
- when the flip-flop switch is in the wake state (ON), arousal system are active and vlPOA is inhibited =>person is awake
- when the flip-flop is in the sleep state (OFF), vlPOA is active, arousal systems are inhibited, person is asleep

Question 94

Physiological mechanisms of sleep and waking

Which arousal neurons are involved in the flip-flop switch and what happens during the ON/OFF periods?

neural control of sleep transitions

Answer 94

Flip-flop on: the arousal areas are activated and when they are activated they inhibit the vlPOA (ventrolateral preoptic area) and when you fall asleep…
flip-flop off: vlPOA is activated and inhibites the areas of arousal that turn on the arousal chemicals

OREXIN ISN’T INCLUDED ONLY THE OTHER 4 AROUSAL CHEMICALS ARE ACTIVATED AND INHIBITED

Question 95

Physiological mechanisms of sleep and waking

Is orexin involved in the flip-flop switch?

neural control of sleep transitions

Answer 95

Orexin isn’t part of the arousal system in this case but instead its role is to keep the switch either on when orexin levels are high, even when adenosine is activated and we’re getting sleepy, orexin keeps it on and activates the chemicals trying to keep us awake
-> motivation to remain awake or events that disturb sleeep activate orexinergic neurons in the lateral hypothalamus which holds flip-flop “on”
=> helps stabilize teh sleep/waking flip-flop through their excitatory connections to the wakefulness neurons
=> activity of this sytem of neurons tips the activity of the flip-flop toward the wking state, thus promoting wakefulness and inhibiting sleep
e.g.: staying awake during boring lecture could depend on maintaining a high rate of firing of orexinergic neurons, which would keep the flip-flop in the waking state

Question 96

Physiological mechanisms of sleep and waking

Why is the flip-flop switch important?

neural control of sleep transitions

Answer 96

it keeps the stability
-> being in a state of sleep and wakefulness would be maladaptive

Question 97

Physiological mechanisms of sleep and waking

What would happen if flip-flop switch was unstable?

neural control of sleep transitions

Answer 97

-> great difficulty remaining awake when nothing interesting is happening
-> have trouble remaining asleep for an extende amount of time
-> show intrusions of the characteristics of REM sleep at inappropriate times (narcolepsy)

Question 98

Physiological mechanisms of sleep and waking

Which arousal neuron is involved in all 3 factors that control sleep and wakefulness (homeostatic, allostatic and circadian?

neural control of sleep transitions

Answer 98

orexin-releasing neurons

Question 99

Physiological mechanisms of sleep and waking

What controls SWS? What factors are involved? What do they influence?

neural control of sleep transitions

Answer 99

-> Lateral hypothalamus receives input from all types of controlling factors: homeostatic, allostatic and circadian rhythm
-> circadan rhythm input on LH: when it’s dark out, its input will signal it’s time to go to sleep so acts on LH same for when it’s daytime
-> homeostatic control (hunger and satiety signals): if hunger gets amplified it is increased, if you’re satiated, then orexin decreases and holds down the arousal signals more weakly => hungry (stay awake); satiated (you can sleep=>inhibit)
-> allostatic factor: adenosine build-up so there’s inhibition => vlPOA sends inhibitory input to orexinergic neurons

Question 100

Physiological mechanisms of sleep and waking

What controls REM sleep transition and sleep? Which neurons are involved?

neural control of sleep transitions

Answer 100

acetylcholinergis neurons
-> play important role in cerebral activation during alert wakefulness
-> involved in neocortical activation that accomapnies REM sleep

sleep/waking flip-flop determines when we wake and when we sleep, once we fall asleep, a second REM flip-flop controls our cycles of REM sleep and SWS
-> once we fall asleep, the activity of orexinergic neurons ceases, which removes one source of the excitatory input to the REM-OFF region
-> as sleep progresses, teh activity of noradregenric and serotonergic neurons gradually decreases => more of the excitatory input to the REM-OFF region is removed => the REM flip-flop tips to the on stage and REM sleep begins
-> this REM switch only becomes important if you’re already asleep, you wanna be asleep to be going through the REM stages

Question 101

Physiological mechanisms of sleep and waking

Is the rate of cerebral metabolism during REM sleep higher or lower than during waking?

neural control of sleep transitions

Answer 101

just as high as during waking

heheh fooled yaa tricky tricky

Question 102

Physiological mechanisms of sleep and waking

Does ACh cause REM?

neural control of sleep transitions

Answer 102

no, but it’s involved in REM (bi-product)

tricked ya again HAHAHHA

Question 103

Physiological mechanisms of sleep and waking

Where are the REM-ON neurons and REM-OFF neurons located? Role?

neural control of sleep transitions

Answer 103

REM-ON neurons: found in sublaterodorsal nucleus (SLD): region of the dorsal pons, just ventral to the locus coeruleus that forms the REM-ON portion of the REM sleep flip-flop
-> in REM: ACh is increased for cortical desynchrony and SLD is activated
-> high rates of firing during REM sleep

REM-OFF neurons: found in ventrolateral periaqueductal gray matter (vlPAG): A region of the dorsal midbrain that forms the REM-OFF portion of the REM sleep flip-flop
-> there neurons are not in REM sleep they are stimulated when vlPAG is activated to suppress REM sleep

when entering REM sleep, vlPAG is inhibited which activates the SLD which inhibits the vlPAG (mutual inhibition) and so on => you’re always in one or the other not both so never in SWS and REM sleep

Question 104

Physiological mechanisms of sleep and waking

What interconnects REM-ON/OFF neurons?

neural control of sleep transitions

Answer 104

inhibitory GABAergic neurons

Question 105

Physiological mechanisms of sleep and waking

Where can the ACh neurons involved in the initiation of REM sleep be found?

neural control of sleep transitions

Answer 105

Peribrachial Area

Question 106

Physiological mechanisms of sleep and waking

Why is the lateral hypothalamus important to sleep?

neural control of sleep transitions

hint: switches

Answer 106

LH keeps the sleep/wake flp-flop switch on and the REM flip-flop switch off
-> without LH’s input, you can experience REM-ON when you’re awake = paralysis

Question 107

Physiological mechanisms of sleep and waking

Does orexin influence both ventrolateral periaquaductal gray matter and sublaterodorsal nucleus?

neural control of sleep transitions

Answer 107

Only influences vlPAG which in turn influences SLD

Question 108

Physiological mechanisms of sleep and waking

What do REM-ON cells do when they’re activated?

neural control of sleep transitions

Answer 108

-> ACh is activated in the forebrain and pons which causes cortical arousal and in lateral preoptic area results in genital activity during REM and also activates tectum, causing rapid eye movements
+
-> REM-ON cells located in sublaterodorsal nucleus fire which cause the inhibitory interneurons in spinal cord to inhibit motor neurons to paralyse us so that we can’t respond to the motor cortex signals in the course of a dream

Question 109

Physiological mechanisms of sleep and waking

What would happen if there was damage in the REM-ON region?

neural control of sleep transitions

Answer 109

No more motor inhibition and individual acts out dreams physically instead of experiencing muscle paralysis during REM sleep

Question 110

Physiological mechanisms of sleep and waking

Narcolepsy and REM flip-flop switch

neural control of sleep transitions

Answer 110

Degeneration of orexinergic neurons in narcolepsy destabilizes the REM flip-flop, making it easier to tip the REM flip-flop into the on sate even during waking which results in cataplexy

Question 111

Physiological mechanisms of sleep and waking

SUMMARY of flip-flop circuits

neural control of sleep transitions

Answer 111

-> If you’re awake then pons, medial septum, basal forebrain and all the arousal systems are activated producing the chemicals to keep SWS on and you stay awake
-> As you get sleepy, arousal system is getting turned off and vlPOA are shutting down the LH and when you go to sleep, LH turns off which turns off the arousal systems which turns off the vlPOA which allows the SWS to turn off so you enter sleep stage 2 and down the SWS stages
-> Inhibition of LH and eventually there will be ninhibition of REM-off area (vlPAG by vlPOA) and once the vlPAG is turned off by vlPOA, it removes the inhibition of the SLD and REM starts which inhibits the vlPAG. Meanwhile teh SLD activates the brain regions that control components of REM sleep
-> Eventually SLD turns off, vlPAG turns back on and vice versa, continues like that during sleep
-> The amygdala can activate the SLD which means that if emotional stimuli enters the amygdala, it can activate REm sleep BUT in typical cases, it doesn’t have much of an effect on SLD aka REM so when we experience something really emotional we don’t just go in SLD bcs the pathway gets inhibited by LH HOWEVER narcolepsy exception

Question 112

Physiological mechanisms of sleep and waking

Humour and narcolepsy

neural control of sleep transitions

Answer 112

-> loss of orexinergic neurons removed an inhibitory influence of HYP on AMYG
-> cases of people that find something so hysterically funny that suddenly became unconscious
-> increased AMYG activity could account at least in part for increased activity of REM-ON neurons that occurs even during waking in people with cataplexy

Question 113

Sleep Disorders

What is insomnia? What types of insomnia are there? Diagnosis? Treatment?

Answer 113

Insomnia: difficulty falling asleep after going to bed or after awakening during the night
-> self-diagnosed insomnia isn’t actually insomnia most of the time

Types:
-> primary insomnia: difficulty falling asleep after going to bed or after awakening during the night (insomnia is the cause of your problems)
-> secondary insomnia: inability to sleep due to another mental or physical condition, such as pain, substance use or a psychological or neurological condition (insomnia is a side-effect of something else)

Diagnosing:
-> challenge of self-report: most pateitns who receive a prescription for a sleeping medication are given one on the basis of their own description of their symptoms
- few patients are observed in night sleep laboratory
- people who report insomnia underestimate the amount of time they actually sleep
- many people experience a sleep-deprived state not bcs they suffer from insomnia but bcs their daily schedules lead them to stay up late or get up early (or both), resulting in less than the optimal amount of sleep
- chronic sleep deprivation can lead to serious health problems, including increased risk of obesity, diabetes and cardiovascular disease

Treatment:
-> nonpharmacological interventions: cognitive behavior therapy (CBT), progressive relaxation techniques and changes in sleep hygiene (maintaining a consistent sleep schedule like waking up and going to sleep at the same time each day)
- keep bedrooms dark, quiet, cool
- this should be main focus bcs sleeping medication (pharmacological interventions) is the most dependent medication known to peoople, we become very dependent on them (cuz sleep is a need and its enjoyable so we get easily addicted to medication for it)
-> pharmacological interventions: include GABA receptor agonists and class of drugs (hypnotics): zolpidem (Ambien) or zaleplon (Sonata)
- also, benzodiapenes and over-the-counter antihistamines such as diphenhydramine which can produce side effects such as sleepiness or difficulty concentrating the following day
- chronic use of sleep-promoting drugs can lead to tolerance and rebound incomnia (return and increase in insomnia) when their use is ended
- e.g.: Michael Jackson was so dependent on sleeping medication (ridiculously huge amount of medication given by his doctor) => died

Question 114

Sleep Disorders

What is sleep apnea? Treatment?

Answer 114

Cessation of breathing intermittenly while sleeping very often, gasping for air
-> nearly all people, especially people who snore, have occasional episodes of sleep apnea, but not to the extent that it interferes with sleep
-> Bcs sleep is disrupted, people with this disorder typically feel sleepy and groggy during the day bcs it interferes with your sleep, causes you to wake up but you wouldn’t necessarily remember why he keeps waking up
Treatment:
-> Fortunately, many cases of sleep apnea are caused by an obstruction of the airway that can be corrected surgically
-> relieved by a device that attacches to the sleeper’s face and provides pressurized air that keeps the airway open
-> sleep on the side

Question 115

Sleep Disorders

What is narcolepsy? Symptoms?

Answer 115

Neurological sleep disorder characterized by periods of irresistible sleep (or some of its components), attacks of cataplexy, sleep paralysis, and hypnagogic hallucinations at inapprorpiate times
-> results of changes in the orexin system

Symptoms:
-> sleep attacks: primary symptom of narcolepsy; irresitible urge to sleep during the day after which person wakes up feeling refreshed
- can happen at any time but occurs most often under monotonous, boring conditions
- sleep generally lasts for 2-5 minutes
-> cataplexy: symptom of narcolepsy; complete paralysis that occurs during waking
- person experiences varying amounts of muscle weakness
- in some cases the person will become completely paralyzed and slump down to the floor. Person will be there, fully conscious, for a few seconds to several minutes. In this situation, one of the phenomena of REM sleep - muscular paralysis-occurs at an inappropriate time. This loss of muscle tone is caused by massive inhibition of motor neurons in the spinal cord. When this happens during waking, the person loses control of his or her muscles. As in REM sleep, the person continues to breathe and is able to control eye movements
- caused by a precipitation in strong emotional reactions or by sudden physical effort: laughter, anger, effort to catch a suddenly thrown obkect

Peopple with narcolepsy try to avoid thoughts and situations that are likely to evoke strong emotions bcs they know that these emotions are more likely to trigger cataplectic attacks

->Sleep paralysis: paralysis occuring just before a person falls asleep => inability to move just before the onset of sleep or on waking in the morning
- REM sleep paralysis sometimes intrudes into waking, such as just befre or just after normal sleep
- person can be snapped out of sleep paralysis by being touched or by hearing someone call their name
- sometimes, mental components of REM sleep intrude into sleep paralysis as well: person might dream while lying awake, paralyzed
- hypnagocic hallucinations: symptom of narcolepsy; vivid dreams that occur just before a person falls asleep, accompanied by sleep paralysis: alarming and terrifying (person experiencing this thought his roomate was trying to kill him)

Question 116

Disorders of Sleep

What is the physiological basis of narcolepsy? Treatment?

Answer 116

-> rare
-> caused by a hereditary autoimmune disorder: most patients with narcolepsy are born with orexinergic neurons, but during adolescence the immune system attacks these neurons, and the symptoms of narcolepsy begin

Treatment:
-> drugs: stimulants (ritalin and catecholamine agonist) or antidepressant drugs (can alleviate REM sleep phenomena which facilitate both serotonergic and noradrenergic activity)
-> most used stimulant: modafinil

Question 117

Sleep Disorders

What is REM sleep behaviour disorder? Characteristics? Treatment? Symptoms?

Answer 117

Neurological disorder in which the person doesn’t become paralyzed during REM sleep and thus acts out dreams
-> maybe SLD doesn’t activate inhibitory interneurons (properly) or the interneurons aren’t inhibiting the motor neurons

Characteristics:
-> neurological disorder where paralysis doesn,t occur during REM sleep
-> neurodegenrative disorder with some genetic component often associated with better-known neurodegenerative disorders such as Parkinson’s disease

Symptoms:
-> opoosite of those of cataplexy => instead of exhibiting paralysis outside REM sleep, patients with REM sleep behaviour disorder fail to exhibit paraysis during REM sleep

Treatments:
-> drug clonazepem: benzodiapezine
-> drugs for cataplexy will worsen the symptoms of REM sleep behaviour disorder

Question 118

Sleep Disorders

What are the disorders associated with REM sleep?

Answer 118

Insomnia, sleep apnea, narcolepsy, REM sleep behaviour disorder

Question 119

Sleep Disorders

What are the disorders associated with SWS? Symptoms? Treatments?

hint: 3 happen in children

Answer 119

3 most frequently happen in children:
-> Bedwetting (nocturnal enuresis): can be cured by training methods like having a special electronic circuit ring a bell when the first few drops of urine are detected in the bed sheet
-> **Night terrors **(pavor nocturnus): anguished screams, trembling, rapid pulse, usually no memory of what caused the terror
-> sleepwalking (somnambulism): not acting out a dream (not related to REM sleep)
- when it occurs in adulthood it’s usualy due to a genetic component
- sometimes people engage in complex behaviours when sleepwalking
-> night terrors and somnambulism usually resolve as the child gets older

-> Sleep-related eating disorder: person leaves their bed and seeks out and eats food while sleepwalking, usually without a memory for the episode the next day
- leave mess and have no recollection of what happened
- happens often
- once they realize what’s happening: employ stratagems such as keeping their food under lock and key or setting alarms that will awaken them when they try to open their fridge
- treatments: dopaminergic agonists or topiramate (anti seizure medication), and may be provoked by zolpidem (benzodiazepine agonist also used totreat insomnia)
- heredity might play a role