Sleep Physiology Exam 2

Q: What are small clusters of neurons in the brain called?

A: Brain nuclei

Q: What is an example of a brain nucleus and its role?

A: The suprachiasmatic nucleus (SCN) helps control the biological clock

Q: How do neurotransmitters transmit signals between neurons?

A: A neuron releases neurotransmitters into the synapse, which bind receptors on the next neuron to pass along the message

Q: How do wake-promoting neurons promote wakefulness?

A: They release neurotransmitters that stimulate the cerebral cortex and other brain regions

Q: What is the ARAS?

A: The Ascending Reticular Activating System—a network of various neuronal types and neurotransmitter pathways

Q: What are three major functions of the ARAS?

A: (1) Arousal and wakefulness, (2) Filtering sensory information, and (3) Sleep-wake regulation

Q: Where does the ARAS originate?

A: In the reticular formation of the brainstem

Q: What is the role of the thalamus in the ARAS?

A: It acts as a relay center for sensory information to ensure input reaches the cortex for wakefulness

Q: What are cortical connections of the ARAS?

A: It sends signals directly and indirectly (via the thalamus) to the cerebral cortex

Q: What other regions are part of the ARAS?

A: Nuclei in the hypothalamus and basal forebrain that are involved in the regulation of wakefulness

Q: What are aminergic pathways? AWAKE

A: Brainstem pathways using monoamines as neurotransmitters that project to the forebrain via the hypothalamus

Q: Where is the noradrenergic system located and what does it release? AWAKE

A: Located in the locus coeruleus; releases norepinephrine

Q: What is the function of the noradrenergic system?

A: Promotes wakefulness and alertness; active during wakefulness and NREM; decreases in REM

Q: Where is the serotonergic system located and what neurotransmitter does it use? AWAKE

A: In the raphe nuclei; uses serotonin (5-HT)

Q: What is serotonin’s activity pattern across sleep stages?

A: High during wakefulness and NREM, decreases during REM; modulates sleep stage transitions

Q: Where is the histaminergic system located and what does it release?

A: Tuberomammillary nucleus; releases histamine

Q: What is histamine’s role in sleep-wake regulation?

A: Promotes wakefulness and alertness; activity drops during sleep, especially REM

Q: Where is the dopaminergic system located and what is its function?

A: Ventral tegmental area; promotes arousal and cognitive alertness

Q: What do cholinergic pathways use and where do they project?

A: Use acetylcholine; project dorsally to the thalamus

Q: Where are the PPT and LDT located and what do they release?

A: In the midbrain and pons; release acetylcholine (ACh)

Q: What does high cholinergic tone indicate?

A: It marks wake and REM states, supporting cortical activation

Q: What is the function of the parabrachial nucleus (PBN)?

A: Promotes wakefulness via excitatory glutamate signals to hypothalamus, forebrain, and cortex

Q: What neurotransmitter do orexin neurons release and what is their role?

A: Release orexin (hypocretin); stabilize wakefulness and prevent inappropriate sleep transitions

Q: What is the primary sleep-promoting region of the brain?

A: The ventrolateral preoptic area (VLPO)

Q: How do VLPO neurons promote sleep?

A: They inhibit wake-promoting neurons in the hypothalamus and brainstem

Q: What is the function of the median preoptic nucleus (MnPO)?

A: Works with the VLPO, contributes to homeostatic sleep drive, and activates earlier

Q: What do VLPO and MnPO neurons co-release and inhibit?

A: Co-release GABA and galanin; inhibit wake-promoting nuclei (LC, TMN, Raphe, LDT/PPT, Orexin)

Q: Where is the sublateral dorsal region (SLD) located and when is it active?

A: In the pons; active during REM sleep

Q: What is the neurotransmitter of SLD and its function?

A: Glutamate; initiates REM and produces atonia via inhibitory medullary pathways

Q: What is the function of the PBc(Glutamate) in REM regulation?

A: Activates forebrain REM EEG patterns and helps switch NREM to REM

Q: What happens when the sleep-wake switch favors wakefulness?

A: Wake-promoting systems activate; sleep-promoting systems are inhibited

Q: What happens when the balance shifts toward sleep?

A: Sleep-promoting neurons inhibit wake-promoting systems

Q: What neurotransmitters maintain wakefulness?

A: Norepinephrine, histamine, dopamine, serotonin, acetylcholine

Q: What neurotransmitter promotes sleep in VLPO?

A: GABA

Q: What role does orexin play in the sleep-wake switch?

A: Acts as a stabilizer by exciting wake neurons and inhibiting sleep-promoting regions

Q: What happens when REM-off neurons are active?

A: REM sleep cannot occur

Q: What happens when REM-off neurons are inactive?

A: REM-on neurons can fire, and REM sleep begins

Q: What happens when REM-on neurons are active?

A: REM sleep occurs

Q: What happens when REM-on neurons are off?

A: REM sleep stops

Q: Where are REM-off regions located?

A: In the midbrain and dorsal pons (vlPAG and LPT)

Q: Where is the REM-on region located and what does it do?

A: The sublaterodorsal nucleus (SLD); drives PGO waves and muscle atonia during REM

Q: Which neurotransmitters are released by REM-off neurons?

A: Orexin, serotonin, and norepinephrine

Q: What effect do REM-off neurotransmitters have?

A: Excite REM-off neurons and inhibit REM-on neurons

Q: Which neurotransmitters activate REM-on neurons?

A: Acetylcholine from the LDT and PPT

Q: What do acetylcholine-releasing neurons do during REM sleep?

A: Excite REM-on neurons and inhibit REM-off neurons, promoting REM sleep

Q: What are sawtooth waves?

A: Distinctive EEG waveforms seen during REM sleep, especially before bursts of rapid eye movement

Q: What are PGO waves?

A: Ponto-geniculo-occipital waves seen during REM sleep, moving from the pons to the thalamus to the occipital lobe

Q: When do PGO waves appear?

A: Just before and during REM sleep

Q: What are PGO waves associated with?

A: The most vivid dreaming stage of sleep

Q: What is the function of PGO waves?

A: They help generate visual imagery during dreams and may aid emotional and visual memory consolidation

Q: Where are PGO waves generated and where do they propagate?

A: Generated in the pons, move to the lateral geniculate nucleus (LGN), and then to the occipital cortex

Q: What is blocked during REM sleep while PGO waves are active?

A: External sensory input and motor output

Q: What do clusters of PGO waves indicate?

A: They occur during REM sleep and mark transitions from NREM to REM

Q: What happens to aminergic activity during REM onset?

A: It declines (serotonin and norepinephrine decrease)

Q: What happens to cholinergic activity during REM onset?

A: It rises, promoting PGO waves and cortical activation

Q: What is adenosine?

A: A neuromodulator formed from ATP breakdown during neuronal and glial energy use

Q: How do adenosine levels change across the day?

A: They rise during wakefulness and fall during sleep

Q: Where does adenosine especially accumulate?

A: In the basal forebrain and preoptic area

Q: How does adenosine promote sleep?

A: By inhibiting wake-promoting cholinergic neurons in the basal forebrain and exciting sleep-active VLPO neurons

Q: What happens to adenosine when the brain is awake and metabolically active?

A: ATP is used, adenosine builds up, increasing sleep pressure

Q: When do adenosine levels drop?

A: During sleep

Q: How does caffeine promote alertness?

A: By blocking adenosine receptors

Q: What effect does blocking adenosine signaling have?

A: It reduces fatigue-promoting signals and increases alertness

Q: What happened to hit rate after sleep deprivation?

A: It decreased, but returned to baseline after one night of recovery

Q: What happened to false positive rate after sleep deprivation?

A: It increased, but returned to baseline after one night of recovery

Q: What is the Psychomotor Vigilance Test (PVT)?

A: A test measuring alertness, attention, and reaction time in response to visual stimuli

Q: What are the key features measured by PVT?

A: Response speed, lapses (slow/no response), and false alarms (response with no stimulus)

Q: Which tasks are more sensitive to sleep loss, visual or auditory?

A: Visual vigilance tasks

Q: How did reaction time and errors change with longer wakefulness?

A: Both increased, especially after 16–24 hours without sleep

Q: How did task demands affect performance during sleep deprivation?

A: More demanding tasks (triple) worsened performance more than simple tasks

Q: What does sleep deprivation especially impair?

A: Divided attention and multitasking ability

Q: Did performance on the PVT fully recover after 3 days of recovery sleep?

A: No, performance deficits persisted

Q: Did subjective sleepiness recover after 3 days?

A: Yes, people felt rested even though objective performance was still poor

Q: What does this suggest about weekend catch-up sleep?

A: It’s not sufficient to restore full performance

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A: Cognitive deficits accumulated across days

Q: How severe were deficits after 14 days of 6-hour sleep?

A: Nearly as severe as total sleep deprivation

Q: When do fatigue-related truck accidents peak?

A: Early morning hours (around 3–8 AM)

Q: Why do fatigue-related crashes peak in the early morning?

A: This time aligns with the circadian low point, increasing crash risk

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A: During extended overnight shifts

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A: Fewer serious errors, preventable adverse events, and attentional failures

Q: How did performance change with wakefulness and BAC?

A: It declined linearly in both conditions

Q: What improvements came from sleep extension?

A: Faster sprints, more accurate shots, and better self-rated performance

Q: How does prior wakefulness duration influence performance?

A: Longer wakefulness worsens performance

Q: Which time of day is more affected by sleep loss?

A: Afternoon performance is more negatively impacted than morning

Q: How does insufficient sleep affect attention and memory?

A: It decreases attention, impairs memory, and slows processing

Q: What sleep duration was linked to negative outcomes in teens?

A: Less than 8 hours

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A: More depression, caffeine use, and substance use risk

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A: 70% reduction in car crashes (7:35 AM → 8:55 AM)

A: Sleep and academic performance in MIT chemistry students

A: Greater amount, better quality, earlier bedtime

Q: What is sleep inertia?

A: Grogginess and impaired performance immediately after waking

Q: How long can sleep inertia last?

A: From a few minutes to 30+ minutes

Q: What does the Three-Process Model integrate?

A: Sleep inertia, homeostatic, and circadian influences on cognition and behavior

Q: In Van Dongen et al. (2003), when was performance lowest?

A: Immediately upon awakening

Q: How quickly did performance improve after waking?

A: Rapidly within the first hour

Q: Was performance after 26 hours awake lower than right after waking?

A: No, post-awakening performance was worse

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A: Within the first 1–2 hours after waking

Q: When do accident rates approach baseline after waking?

A: After ~4–5 hours awake

Q: Why is sleep inertia a safety risk?

A: It temporarily impairs cognition and reaction more than later fatigue

Q: What are major health risks of sleeping less than 6–7 hours per night?

A: Weight gain and obesity, type 2 diabetes, cardiovascular disease and stroke, increased pain, cancer, and Alzheimer’s disease

Q: What was the main finding of Hasler et al. (2004)?

A: Shorter sleep duration was linked to a higher risk of obesity