HMB200H1 Study Guide - Final Guide: Ion, Cataplexy, Glossopharyngeal Nerve
1. What is a biorhythm? What terminology do we use to refer to biorhythms of
varying length?
Biorhythm is a variation in a biological process that repeats over a period
of time
Circadian rhythm is 24 hrs. / Biological rhythm is more day a day and
less than a year / Infradian rhythm is shorter than a day.
○
-
2. What do we mean when we say a biorhythm is internal? What is a free-running
rhythm?
Biorhythms are internal as they persist in the absence of cues such as light
Free running rhythms is essentially a biorhythm which exists
endogenously
○
-
3. Describe how biorhythms might shift in constant lighting conditions. Describe
how biorhythms might shift if we receive light at during the sleep phase of our
sleep-wake cycle (e.g. light at night).
Constant light: humans will have shorter sleep-wake cycle
(nocturnal :longer)
-
Constant darkness: humans will have longer sleep-wake cycle (nocturnal:
shorter)
-
4. Describe the process of biorhythm entrainment to light from start to finish.
Biorhythms are set by cues known as zeitgebers. If a biorhythm is set to
the zeigeber, it is entrained. Therefore, if light is the zeitgeber for sleep
wake, we become entrained to the sunset. This occurs as retinal ganglion
cells send signals via the retinohypothalamic tract to the SCN to the
hypothalamus core and ultimately send signals to shell region. This
process is disrupted in light pollution, jet lag and night work
-
5. How does suprachiasmatic nucleus (SCN) lesion affect biorhythm? What about
SCN transplant after lesion?
Lesion of SCN leads to loss of many circadian rhythms. This can be revered
by transplanting a healthy SCN from another animal.
-
6. Explain synchronization at the molecular level.
At the molecular level, PER and CRY protein dimerize and inhibit the
expression of CLOCK-BMAL factor (normally responsible for activating PER
and CRY transcription) which ultimately activates PER and CRY
transcription
-
7. What is delayed sleep phase disorder? What is a risk factor for this disorder?
Delayed sleep phase disorder is when there is a mutation in CRY1 gene
which is involved in the entrainment of our biorhythms. This disorder
makes one goes to bed later and rise later.
-
8. Explain the relationship between the SCN, melatonin and cortisol.
SCN activity peaks during daytime. Cortisol peaks with waking phase
(cortisol awakening response) ad Melatonin peaks at sleeping phase (rise
at initiation of sleep)
-
9. Explain the modulation of SCN activity by other sources. Pay specific attention
to the role of exercise.
Photic input (light) involves glutamate and pituitary adenylate cyclase
activating peptide (PACAP)
Daylight later -> phase delay (sleep later) / Daylight early -> phase
advance
○
-
Non-photic input (exercise) involves dorsal raphe (DRN) and median raphe
(MRN) as well as intergeniculate leaflet (IGL)
Late exercise forces SCN to phase delay (sleep later) while early
exercise leads to phase advance (sleep earlier)
○
-
10.Explain the relationship between grade-point average (GPA), sleep regularity
index (SRI) and dim light melatonin onset (DLMO).
GPA and SRI are positively correlated
-
GPA and DLMO are negatively correlated
-
11.Explain the significance of the reticular formation and dorsal pontine reticular
formation to arousal/wakefulness.
Reticular formation causes arousal
-
Dorsal pontine reticular formation injury leads to comma (loss of
consciousness)
-
12.Why do we need sleep?
Maintenance of brain (waste clearance)
-
Restoration of injured/damaged tissue
-
Ontogenetic development of brain
-
Maintenance of learning and memory processes
-
13.What are the stages of sleep? Explain sleep stage cycling.
NREM 1, NREM 2, NREM 3/4, REM. The cycle begins with rapid decline to
NREM 4 then within the night a constant cycling between NREM 3/4 and
REM with occasional awakenings
-
14.How does sleep change with age?
As we get older, long latency to fall asleep which leads to shorter REM
periods and more frequent bouts of arousal.
-
Biggest age-dependent change: stage 3 sleep
-
15.Explain the role of specific nuclei in the waking EEG, REM EEG and REM atonia.
Waking EEG: increased cholinergic and raphe nuclei (if moving) activity
-
REM EEG: Peribrachial area initiates sleep -> medial pontine reticular
formation create REM related activities. Loss of muscle tone produced by
subcoerulear nucleus exiting the magnocellular nucleus of medulla ->
inhibit spinal motor neurons
-
REM atonia: subcoerulear nucleus excites ventral Gigantocellular reticular
nucleus (GiV) which inhibits skeletal motor neurons
-
16.Is REM necessary for survival? What happens with REM deprivation?
If REM deprivation, then reduced hippocampal neurogenesis, immune
dysfunction and mood disruption. Prolonged REM deprivation results in
REM rebound. REM is necessary for quality of life but not necessarily
survival.
-
17.When do we dream? Why do we dream?
We dream during REM sleep. Purpose is unclear but we might dream
because of wish fulfillment or as a coping strategy. Based on Activation
Synthesis Theory of Dreaming, dream states are attempt of brain to
interpret ransom neural activity.
-
18.Contrast subjective and objective analysis of sleep behavior.
Subjective: surveying the patients about their sleep patterns with
questionnaires
-
Objective: Observing neurological and physiological activity during sleep
(EEG)
-
19.Explain the neural correlates of sleep disorders.
Insomnia: difficulty falling asleep or staying asleep. Acute or chronic and it
is commonly comorbid with other disorders (heart disease, depression,
etc.)
-
Cataplexy: loss of motor control (atonia) without loss of consciousness
which occurs due to damage to orexin-expressing neurons in lateral
hypothalamus which is suppose to inhibit neurons that initiate atonia
Narcolepsy: daytime sleepiness and frequent dozing + rapid REM
descent. Treat with amphetamine or GABA agonist or orexin /
hyprocretin peptide
○
-
Somnambulism: sleep walking, occur during NREM
-
Apnoea: breathing difficulties during sleep result in low concentration of
oxygenation of blood, repeated awakenings.
-
20.What is the relationship between sleep deprivation and obesity?
The ventrolateral preoptic nucleus (VLPO) inhibits the orexin system in
lateral hypothalamus which prevents a number of events
Sleep deprivation is associated with weight gain and immune
dysfunction
○
-
21.Explain the role of taste receptors in taste.
Taste receptors allow for the sensation of 5 tastes, sweet (sucrose), salty
(sodium chloride), sour (citric acid), bitter (quinine) and umami (glutamic
acid)
GPCRs: sweet, bitter, umami
○
Ion channel: salty and sour (Na+ and H+)
○
-
22.Explain our ability to recognize spicy foods.
Capsaicinoids from spicy food activates the transient receptor potential
cation channel subfamily V type 1 (TRPV1) receptor (Vanillioid / VR1
receptors)
-
23.Give the organization of the taste pathway from start to finish.
Taste cells -> CN 7, 9, 10 -> thalamus -> insula + somatosensory cortex
CN 7: facial nerve
○
CN 9: Glossopharyngeal nerve
○
CN 10: Vagus nerve
○
-
24.What is the neural evidence for super-tasting?
Variations in gustin gene and TAS2R38 gene show evidence in supertaster
theory. Those with certain TAS2R38 alleles are revolted by bitter tastes
due to increased sensitivity. Super tasting may also be on account of the
increased number of taste buds (fungiform) in supertasters.
-
25.What is the olfactory pathway from start to finish?
Olfactory receptors
Olfactory bulbs
Amygdala
§
Prepyriform cortex (as well as olfactory tubercle, entorhinal
cortex)
Hypothalamus □
Medial dorsal thalamus
Lateral posterior orbitofrontal cortex
®
Orbitofrontal cortex (as well as limbic cortex)
®
□
§
○
-
26.What some theories about how we smell?
Shape theory: odorants activate specific odorant receptors that are
receptive to their particular shape
-
Vibrational theory: vibration energy
-
27.Do humans have a worse sense of smell than animals? What is the evidence?
Humans have smaller olfactory bulbs but similar amounts of olfactory
neurons as animals. Differences in genetic expression and elevation form
ground are factors in the sensitivity to odorants. Humans can be trained to
track scent, but we still can't compare to dogs
-
Study notes 9
Thursday, April 5, 2018
10:13 PM
1. What is a biorhythm? What terminology do we use to refer to biorhythms of
varying length?
Biorhythm is a variation in a biological process that repeats over a period
of time
Circadian rhythm is 24 hrs. / Biological rhythm is more day a day and
less than a year / Infradian rhythm is shorter than a day.
○
-
2. What do we mean when we say a biorhythm is internal? What is a free-running
rhythm?
Biorhythms are internal as they persist in the absence of cues such as light
Free running rhythms is essentially a biorhythm which exists
endogenously
○
-
3. Describe how biorhythms might shift in constant lighting conditions. Describe
how biorhythms might shift if we receive light at during the sleep phase of our
sleep-wake cycle (e.g. light at night).
Constant light: humans will have shorter sleep-wake cycle
(nocturnal :longer)
-
Constant darkness: humans will have longer sleep-wake cycle (nocturnal:
shorter)
-
4. Describe the process of biorhythm entrainment to light from start to finish.
Biorhythms are set by cues known as zeitgebers. If a biorhythm is set to
the zeigeber, it is entrained. Therefore, if light is the zeitgeber for sleep
wake, we become entrained to the sunset. This occurs as retinal ganglion
cells send signals via the retinohypothalamic tract to the SCN to the
hypothalamus core and ultimately send signals to shell region. This
process is disrupted in light pollution, jet lag and night work
-
5. How does suprachiasmatic nucleus (SCN) lesion affect biorhythm? What about
SCN transplant after lesion?
Lesion of SCN leads to loss of many circadian rhythms. This can be revered
by transplanting a healthy SCN from another animal.
-
6. Explain synchronization at the molecular level.
At the molecular level, PER and CRY protein dimerize and inhibit the
expression of CLOCK-BMAL factor (normally responsible for activating PER
and CRY transcription) which ultimately activates PER and CRY
transcription
-
7. What is delayed sleep phase disorder? What is a risk factor for this disorder?
Delayed sleep phase disorder is when there is a mutation in CRY1 gene
which is involved in the entrainment of our biorhythms. This disorder
makes one goes to bed later and rise later.
-
8. Explain the relationship between the SCN, melatonin and cortisol.
SCN activity peaks during daytime. Cortisol peaks with waking phase
(cortisol awakening response) ad Melatonin peaks at sleeping phase (rise
at initiation of sleep)
-
9. Explain the modulation of SCN activity by other sources. Pay specific attention
to the role of exercise.
Photic input (light) involves glutamate and pituitary adenylate cyclase
activating peptide (PACAP)
Daylight later -> phase delay (sleep later) / Daylight early -> phase
advance
○
-
Non-photic input (exercise) involves dorsal raphe (DRN) and median raphe
(MRN) as well as intergeniculate leaflet (IGL)
Late exercise forces SCN to phase delay (sleep later) while early
exercise leads to phase advance (sleep earlier)
○
-
10.Explain the relationship between grade-point average (GPA), sleep regularity
index (SRI) and dim light melatonin onset (DLMO).
GPA and SRI are positively correlated
-
GPA and DLMO are negatively correlated
-
11.Explain the significance of the reticular formation and dorsal pontine reticular
formation to arousal/wakefulness.
Reticular formation causes arousal
-
Dorsal pontine reticular formation injury leads to comma (loss of
consciousness)
-
12.Why do we need sleep?
Maintenance of brain (waste clearance)
-
Restoration of injured/damaged tissue
-
Ontogenetic development of brain
-
Maintenance of learning and memory processes
-
13.What are the stages of sleep? Explain sleep stage cycling.
NREM 1, NREM 2, NREM 3/4, REM. The cycle begins with rapid decline to
NREM 4 then within the night a constant cycling between NREM 3/4 and
REM with occasional awakenings
-
14.How does sleep change with age?
As we get older, long latency to fall asleep which leads to shorter REM
periods and more frequent bouts of arousal.
-
Biggest age-dependent change: stage 3 sleep
-
15.Explain the role of specific nuclei in the waking EEG, REM EEG and REM atonia.
Waking EEG: increased cholinergic and raphe nuclei (if moving) activity
-
REM EEG: Peribrachial area initiates sleep -> medial pontine reticular
formation create REM related activities. Loss of muscle tone produced by
subcoerulear nucleus exiting the magnocellular nucleus of medulla ->
inhibit spinal motor neurons
-
REM atonia: subcoerulear nucleus excites ventral Gigantocellular reticular
nucleus (GiV) which inhibits skeletal motor neurons
-
16.Is REM necessary for survival? What happens with REM deprivation?
If REM deprivation, then reduced hippocampal neurogenesis, immune
dysfunction and mood disruption. Prolonged REM deprivation results in
REM rebound. REM is necessary for quality of life but not necessarily
survival.
-
17.When do we dream? Why do we dream?
We dream during REM sleep. Purpose is unclear but we might dream
because of wish fulfillment or as a coping strategy. Based on Activation
Synthesis Theory of Dreaming, dream states are attempt of brain to
interpret ransom neural activity.
-
18.Contrast subjective and objective analysis of sleep behavior.
Subjective: surveying the patients about their sleep patterns with
questionnaires
-
Objective: Observing neurological and physiological activity during sleep
(EEG)
-
19.Explain the neural correlates of sleep disorders.
Insomnia: difficulty falling asleep or staying asleep. Acute or chronic and it
is commonly comorbid with other disorders (heart disease, depression,
etc.)
-
Cataplexy: loss of motor control (atonia) without loss of consciousness
which occurs due to damage to orexin-expressing neurons in lateral
hypothalamus which is suppose to inhibit neurons that initiate atonia
Narcolepsy: daytime sleepiness and frequent dozing + rapid REM
descent. Treat with amphetamine or GABA agonist or orexin /
hyprocretin peptide
○
-
Somnambulism: sleep walking, occur during NREM
-
Apnoea: breathing difficulties during sleep result in low concentration of
oxygenation of blood, repeated awakenings.
-
20.What is the relationship between sleep deprivation and obesity?
The ventrolateral preoptic nucleus (VLPO) inhibits the orexin system in
lateral hypothalamus which prevents a number of events
Sleep deprivation is associated with weight gain and immune
dysfunction
○
-
21.Explain the role of taste receptors in taste.
Taste receptors allow for the sensation of 5 tastes, sweet (sucrose), salty
(sodium chloride), sour (citric acid), bitter (quinine) and umami (glutamic
acid)
GPCRs: sweet, bitter, umami
○
Ion channel: salty and sour (Na+ and H+)
○
-
22.Explain our ability to recognize spicy foods.
Capsaicinoids from spicy food activates the transient receptor potential
cation channel subfamily V type 1 (TRPV1) receptor (Vanillioid / VR1
receptors)
-
23.Give the organization of the taste pathway from start to finish.
Taste cells -> CN 7, 9, 10 -> thalamus -> insula + somatosensory cortex
CN 7: facial nerve
○
CN 9: Glossopharyngeal nerve
○
CN 10: Vagus nerve
○
-
24.What is the neural evidence for super-tasting?
Variations in gustin gene and TAS2R38 gene show evidence in supertaster
theory. Those with certain TAS2R38 alleles are revolted by bitter tastes
due to increased sensitivity. Super tasting may also be on account of the
increased number of taste buds (fungiform) in supertasters.
-
25.What is the olfactory pathway from start to finish?
Olfactory receptors
Olfactory bulbs
Amygdala
§
Prepyriform cortex (as well as olfactory tubercle, entorhinal
cortex)
Hypothalamus □
Medial dorsal thalamus
Lateral posterior orbitofrontal cortex
®
Orbitofrontal cortex (as well as limbic cortex)
®
□
§
○
-
26.What some theories about how we smell?
Shape theory: odorants activate specific odorant receptors that are
receptive to their particular shape
-
Vibrational theory: vibration energy
-
27.Do humans have a worse sense of smell than animals? What is the evidence?
Humans have smaller olfactory bulbs but similar amounts of olfactory
neurons as animals. Differences in genetic expression and elevation form
ground are factors in the sensitivity to odorants. Humans can be trained to
track scent, but we still can't compare to dogs
-
Study notes 9
Thursday, April 5, 2018 10:13 PM
