MCB 462 FINAL VERIFIED STUDY GUIDE
Sleeping and the day/night cycle
Light info sent through retinohypothalamic tract to SCN, entrains CR to light at
molecular clock level, modulates sleep cycles (phase shifting)
SCN can modulate melatonin release to promote sleep in diurnal animals
Sleeping and zeitgeibers (time givers)
Zeitgeibers modulare the CR so can alter sleep schedule timing
Typically light is strongest zeitgeiber but ffeding cues may take priority under severe
food restriction
Other inputs: ACh from basal forebrain (learning and arousal) and brainstem, 5-HT from
Raphe (Serotonin directly arouses SCN), forebrain learning, peptides, drugs of abuse
Sleep and homeostasis
Less sleep leads to homeostatic drives to increase sleep pressures, integrated with
circadian wake process
Glymphatic system clears metabolic waste (ex. amyloid Beta) during sleep,
accumulation of waste during sleep deprivation may stimulate homeostatic drive to
sleep
Sleep (esp. REM) may be necessary for memory consolidation
Processes regulating sleep
Intrinsic: circadian and homeostatic
Extrinsic: light/dark cycle, social experience
Ontogenetic life span changes: age
Volition: voluntary sleep curtailment
Processes peripheral to brain that are regulated in sleep
Hormone profiles, endocrine function
Metabolic function
Immune function
Cardiovascular variables
Melanopsin
Photopigment (light sensitive protein) located in the intrinsically photosensitive Retinal
Ganglion Cells (ipRGCs)
, Activates the ipRGCs in response to blue wavelength light, which communicates light
info to SCN via retinohypothalamic tract
ipRGCs
Do not receive or process input from visual photoreceptors
Have diffuse dendritic processes that form a wide melanopsin expressing net that
collects presence of light info
Do not use lateral inhibition
Send light info to SCN via glutamatergic projections that form retinohypothalamic tract
Communication with deep brain regions that regulate mood but do not innervate visual
system
Light during subjective night
Light in early subjective night delays the internal clock by moving it to the late day
Light in late subjective night (generally after midnight) advances the clock to an early
daytime state
Universal characteristics sleep-like state
Absence of voluntary movements
Spontaneous, occurring in circadian rhythm
Reversible, with sensory stimulations vs pathological states (coma, exhaustion)
Increased arousal threshold
Characteristic species-specific posture and/or resting place that minimizes sensory
stimulation
State-related changes in neural function, including decreased sensory input to CNS
Identifiable as a stable species characteristic
Sleep as a plastic behavior
Sleeping individuals are still able to respond to external stimuli (with a higher threshold),
unlike in pathological states (ex. coma)
Can control when, where, and how we sleep
Light and other stimuli are able to cause phase shifts and advance/delays in circadian
rhythm (rapidly changing day/night cycle = jet lag)
Start with more deep sleep at beginning of sleep cycle then decreases as the night goes
on, while REM becomes more pronounced as night goes on
Sleep deprivation affects sleep stages and homeostatic sleep drive - more pronounced
deep sleep in deprived individuals
Sleep cycled change with age, become more fragmented with less consolidated bouts
of sleep
Two process model of sleep
Sleeping and the day/night cycle
Light info sent through retinohypothalamic tract to SCN, entrains CR to light at
molecular clock level, modulates sleep cycles (phase shifting)
SCN can modulate melatonin release to promote sleep in diurnal animals
Sleeping and zeitgeibers (time givers)
Zeitgeibers modulare the CR so can alter sleep schedule timing
Typically light is strongest zeitgeiber but ffeding cues may take priority under severe
food restriction
Other inputs: ACh from basal forebrain (learning and arousal) and brainstem, 5-HT from
Raphe (Serotonin directly arouses SCN), forebrain learning, peptides, drugs of abuse
Sleep and homeostasis
Less sleep leads to homeostatic drives to increase sleep pressures, integrated with
circadian wake process
Glymphatic system clears metabolic waste (ex. amyloid Beta) during sleep,
accumulation of waste during sleep deprivation may stimulate homeostatic drive to
sleep
Sleep (esp. REM) may be necessary for memory consolidation
Processes regulating sleep
Intrinsic: circadian and homeostatic
Extrinsic: light/dark cycle, social experience
Ontogenetic life span changes: age
Volition: voluntary sleep curtailment
Processes peripheral to brain that are regulated in sleep
Hormone profiles, endocrine function
Metabolic function
Immune function
Cardiovascular variables
Melanopsin
Photopigment (light sensitive protein) located in the intrinsically photosensitive Retinal
Ganglion Cells (ipRGCs)
, Activates the ipRGCs in response to blue wavelength light, which communicates light
info to SCN via retinohypothalamic tract
ipRGCs
Do not receive or process input from visual photoreceptors
Have diffuse dendritic processes that form a wide melanopsin expressing net that
collects presence of light info
Do not use lateral inhibition
Send light info to SCN via glutamatergic projections that form retinohypothalamic tract
Communication with deep brain regions that regulate mood but do not innervate visual
system
Light during subjective night
Light in early subjective night delays the internal clock by moving it to the late day
Light in late subjective night (generally after midnight) advances the clock to an early
daytime state
Universal characteristics sleep-like state
Absence of voluntary movements
Spontaneous, occurring in circadian rhythm
Reversible, with sensory stimulations vs pathological states (coma, exhaustion)
Increased arousal threshold
Characteristic species-specific posture and/or resting place that minimizes sensory
stimulation
State-related changes in neural function, including decreased sensory input to CNS
Identifiable as a stable species characteristic
Sleep as a plastic behavior
Sleeping individuals are still able to respond to external stimuli (with a higher threshold),
unlike in pathological states (ex. coma)
Can control when, where, and how we sleep
Light and other stimuli are able to cause phase shifts and advance/delays in circadian
rhythm (rapidly changing day/night cycle = jet lag)
Start with more deep sleep at beginning of sleep cycle then decreases as the night goes
on, while REM becomes more pronounced as night goes on
Sleep deprivation affects sleep stages and homeostatic sleep drive - more pronounced
deep sleep in deprived individuals
Sleep cycled change with age, become more fragmented with less consolidated bouts
of sleep
Two process model of sleep
