Lecture 9 Flashcards

1
Q

Which brain regions show reduced responses in psychopathy when responding to emotional stimuli? (3)

A

The amygdala, anterior insula, and ventromedial prefrontal cortices show reduced responses in psychopathy when responding to emotional stimuli.

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2
Q

What are the key characteristics of psychopathy? (4)

A
  1. Antisocial behavior
  2. Lack of empathy
  3. Lack of remorse
  4. Impulsivity and aggression
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3
Q

During empathy tasks, how does the amygdala’s response to the distress of others differ in individuals with psychopathy compared to typical individuals?

A

In psychopaths, the amygdala reacts less to others’ distress, leading to lower empathy and more use of aggression to achieve goals, unlike typical people.

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4
Q

Why do psychopaths perform poorly on decision-making tasks, and what are the consequences of reduced reinforcement sensitivity?

A

Psychopaths struggle to learn from rewards or punishments due to reduced reinforcement sensitivity, leading to poor decision-making, impulsive behavior, and frustration-induced aggression.

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5
Q

Which brain areas show reduced responsiveness in psychopaths, and what is the consequence?

A

The striatum and ventromedial prefrontal cortex show weaker responses, making it harder for psychopaths to feel the effects of rewards.

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6
Q

How do high psychopathy scores relate to responses in the ventral striatum?

A

High psychopathy scores are linked to reduced ventral striatum activity during monetary loss, showing a lack of emotional response.

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7
Q

Why don’t psychopaths learn to avoid negative consequences after punishment?

A

Psychopaths struggle to learn from punishment because their brain doesn’t reduce activity in key areas (prefrontal and posterior cingulate cortex) after being punished, so they don’t adjust their behavior.

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8
Q

What is the location and primary function of the SCN (suprachiasmatic nucleus)?

A
  • The SCN is located in the hypothalamus
  • Functions as the brain’s molecular clock, regulating the daily biological clock and wake/sleep cycles.
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9
Q

How does light influence the SCN, and what is the molecular mechanism of its function?

A
  • Light activates neurons projecting onto the SCN, initiating circadian regulation.
  • SCN genes (Bmal1 and Clock) produce BMAL1 and CLOCK proteins, which dimerize to drive Per2 and Cry1 transcription, which regulate circadian rhythms.
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10
Q

How do PER and CRY proteins form a feedback loop to regulate the circadian clock?

A
  • PER and CRY proteins accumulate, dimerize, and move into the nucleus, where they inhibit BMAL1 and CLOCK, stopping their own production.
  • As PER and CRY degrade, BMAL1 and CLOCK resume activity, restarting the cycle.
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11
Q

What external factors influence the circadian rhythm?

A

External cues like light and temperature cause fluctuations in BMAL1 and CLOCK levels over a 24-hour cycle.

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12
Q

What is the role of retinal ganglion cells (RGCs) in the circadian system?

A

RGCs are specialized cells in the retina that contain melanopsin, which causes them to depolarize in response to light, transmitting light information to the SCN.

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13
Q

What pathway do light signals travel through to reach the SCN?

A

Light signals travel through the retinohypothalamic tract to reach the SCN, where they inform the circadian rhythm.

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14
Q

What happens to SCN neurons when isolated?

A

SCN neurons continue to exhibit circadian activity even when isolated, showing their inherent rhythmicity.

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15
Q

What are the steps in how light regulates the brain’s clock and melatonin production?

A
  1. Retinal ganglion cells detect light and send signals to the SCN in the hypothalamus.
  2. SCN activation stimulates the paraventricular nucleus (PVN), which sends signals to the spinal cord, activating the superior cervical ganglion
  3. The superior cervical ganglion sends signals to the pineal gland near the dorsal thalamus.
  4. The pineal gland produces melatonin, which regulates sleep-wake cycles, peaking between 2-4 am to promote restorative sleep.
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16
Q

How does hamster activity differ with an intact SCN versus a damaged SCN?

A
  1. With an intact SCN, hamsters display synchronized circadian rhythms tied to the light/dark cycle, as they are naturally nocturnal.
  2. When the SCN is damaged, they lose the ability to regulate these rhythms, and their activity becomes random, especially in dim light.
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17
Q

How does sleep influence the body’s daily biological functions? (3)

A

Sleep regulates a 24-hour biological rhythm, balances physiological needs (homeostasis), and drives fluctuations in temperature, hormones, and cortisol levels.

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18
Q

What are the key restorative and functional roles of sleep? (5)

A
  • Repairs tissues
  • Restocks hormones and glycogen
  • Conserves energy by reducing metabolic demand
  • Aids survival (diurnal/nocturnal behavior)
  • Strengthens memory through consolidation
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19
Q

How are sleep deprivation chambers used to prevent REM sleep in rodents?

A

They rotate a platform periodically, forcing rodents into water to wake them up and prevent REM sleep.

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20
Q

What technology can be used to disrupt sleep stages in rodents?

A

EEG feedback can disrupt different sleep stages during experiments.

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21
Q

What are the effects of 2–3 weeks of sleep deprivation in rats?

A

Sleep deprivation causes weight loss, decreased thermoregulation, immune dysfunction, and eventual death due to a decline in immune function, increased infections, and reduced cortical function.

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22
Q

What are the long-term effects of sleep deprivation on rodents’ brains?

A
  • Degeneration of cortex and thalamus
  • Increased beta load, links to prion and Alzheimer’s disease
    -Diffuse bacterial infections
  • Eventua death within 7-24 months
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23
Q

What were the cognitive effects observed in a human staying awake for 11 days?

A
  • Clear deficits in attention, - Inability to perform simple tasks
  • Cognitive impairments were observed after just 2 days.
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24
Q

What are the long-term effects of sleep deprivation on health?

A

Weight gain/loss, increased risk of diabetes and CVD, impaired cognition, and hallucinations.

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25
Q

How is chronic jet lag associated with brain health?

A

It is linked to reduced temporal lobe volume in airline employees.

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26
Q

What is fatal familial insomnia, and how does it affect individuals?

A

A genetic condition causing hallucinations, seizures, inability to enter deep sleep, and death within years of onset.

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27
Q

What effect does one night of sleep deprivation have on the brain?

A

It increases fibrillar brain amyloid-beta (Aβ) load in the hippocampus, associated with Alzheimer’s disease.

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28
Q

How does sleep protect the brain?

A

Sleep activates the glymphatic system, increasing cerebrospinal fluid (CSF) flow to flush out toxins and waste from the brain.

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29
Q

What does an EEG record?

A

EEG records the summed activity of neuron groups, particularly pyramidal neurons, and detects synchronized neural activity.

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30
Q

What is the primary limitation of EEG recordings?

A

EEG has poor spatial resolution but is effective for monitoring overall cortical activity.

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31
Q

What is unilateral sleep, and why do dolphins use it?

A

Unilateral sleep is when one hemisphere of the brain sleeps while the other stays awake. Dolphins use it to maintain awareness and avoid drowning.

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32
Q

What type of sleep pattern is observed in dolphins during unilateral sleep?

A

Slow-wave sleep with high amplitude and low frequency in one hemisphere.

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33
Q

What brain waves are associated with being awake and focused?

A

When awake, the brain shows high-frequency, low-amplitude alpha waves (calm, relaxed but awake state) and beta waves (associated with active thought or focus).

34
Q

What happens during Stage 1 sleep?

A

Stage 1 sleep is the transition from wakefulness to sleep, where theta waves (low-frequency, higher-amplitude activity) begin to appear.

35
Q

What characterizes Stage 2 sleep?

A

Marked by sleep spindles (short bursts of high-frequency activity) and K-complexes (large waves), which play a role in memory and sleep stability.

36
Q

What role does the thalamus play in sleep spindles?

A

The thalamus is important for generating sleep spindles.

37
Q

What is the function of sleep spindles?

A

Sleep spindles are linked to the brain’s processing of new information, with more occurring when you’ve learned new things.

38
Q

How do eye movements and K complexes change during sleep?

A

Eye movements (saccades) slow down during sleep, and K complexes are thought to help reduce arousal in the brain to help you stay asleep

39
Q

What brain waves characterizes Stage 3 and 4 sleep?

A
  • Involve slow-wave sleep (SWS)
  • Characterized by delta waves, which have low frequency and high amplitude.
40
Q

What is the difference between Stage 3 and Stage 4 of sleep?stage

A

Stage 3: Moderate-deep sleep, starting the body’s recovery process.
Stage 4: Deepest sleep, where the body does the most repair and recovery.

41
Q

What happens after Stage 4 sleep?

A

After Stage 4, the cycle reverses to REM sleep, where the brain is highly active, dreams happen, and the body is temporarily paralyzed to prevent acting them out.

42
Q

How do sleep cycles and quality change with age?

A

Younger people experience longer and deeper sleep cycles, while sleep quality decreases with age, leading to more fragmented sleep.

43
Q

What is Narcolepsy and what happens during a sleep attack?

A

Narcolepsy is a chronic condition where a person suddenly experiences REM sleep “attacks” that can last from 30 seconds to 30 minutes, with vivid dreams or hallucinations.

44
Q

What is cataplexy in Narcolepsy?

A

Cataplexy is the sudden loss of muscle tone, which can happen even while awake and is often triggered by strong emotions

45
Q

How is brain activity affected in people with Insomnia?

A

PET scans show that the ascending arousal activating
system (“alertness” system) is overactive in people with Insomnia, making it harder for them to sleep.

46
Q

What evidence from animal studies supports the understanding of brain activity in Insomnia?

A

Studies on rats exposed to acute stress show high-frequency EEG responses during sleep, which is similar to the increased brain activity observed in humans with Insomnia.

47
Q

What brain changes are linked to Insomnia?

A
  • Increased firing of the locus coeruleus (LC), which is linked to alertness
  • Increased histaminergic drive, which promotes wakefulness, both contributing to sleep difficulties.
48
Q

How is the VLPO involved in the development of insomnia?

A

In insomnia, the VLPO fails to properly suppress the ascending arousal system, leading to excessive brain activity that prevents restful sleep.

49
Q

Why do elderly individuals experience fragmented sleep?

A

Some elderly people lose neurons in the VLPO, impairing their ability to regulate sleep, which results in more frequent awakenings and fragmented sleep.

50
Q

What are the common treatments for insomnia?

A

Include benzodiazepines, which help induce sleep, and Cognitive Behavioral Therapy (CBT), which addresses the root causes of insomnia.

51
Q

What role does orexin play in sleep regulation?

A

Orexin, produced in the posterior lateral hypothalamus, excites neuromodulatory nuclei to help maintain wakefulness and regulate sleep cycles.

52
Q

What causes narcolepsy in terms of orexin function?

A

Caused by a decrease in orexin-secreting neurons or mutations in orexin receptors, leading to disrupted arousal tone.

53
Q

What role does the pontine reticular formation (PRF) play during REM sleep?

A
  1. Blocks LC-mediated motor neuron activation, causing muscle paralysis.
  2. Activates inhibitory interneurons to suppress motor neuron activity, to induce muscle paralysis.
  3. Controls eye movements via signals to the lateral geniculate nucleus and occipital cortex.
54
Q

What causes muscle paralysis during REM sleep?

A

Inhibitory pathways block motor neuron activation and reduce sensory input by inhibiting dorsal column nuclei cells, ensuring the body stays paralyzed while the brain remains active.

55
Q

What causes the emotional intensity of REM dreams?

A

Increased limbic system activity combined with reduced cortical inputs produces emotional intensity in REM dreams.

56
Q

Why do REM dreams often lack logical structure?i

A

The dorsolateral prefrontal cortex, which handles logical and organized thinking, is less active during REM sleep.

57
Q

Which brain regions show increased activity during REM sleep?

A

The amygdala, parahippocampal gyrus, and anterior cingulate cortex have increased activity during REM sleep.

58
Q

How do the RAS and VLPO work together to regulate sleep and wakefulness?

A

The RAS promotes wakefulness by activating cholinergic pathways and shifting brainwaves from delta (sleep) to beta (wake), while the VLPO suppresses the RAS to maintain sleep.

59
Q

What role does the RAS play in maintaining wakefulness, and what are the consequences of its damage?

A

The RAS supports wakefulness by enabling communication between the thalamus and cortex. Damage to the RAS can lead to a coma.

60
Q

What is the activity pattern of cholinergic neurons from the nucleus basalis across different sleep states?

A
  • They are active during wakefulness and REM sleep, but have reduced activity during non-REM sleep.
61
Q

How do cholinergic neurons contribute to the similarity between REM sleep and wakefulness?

A

Their high discharge rates during both states result in overlapping brain activity patterns.

62
Q

What is the function of the locus coeruleus in regulating sleep and wakefulness?

A
  • Produces noradrenergic outputs that promote arousal and alertness,
    -Increase firing in anticipation of waking
  • Decrease activity prior to REM sleep.
63
Q

How does the locus coeruleus contribute to the arousal process after sleep?

A

The locus coeruleus projects throughout the cortex and brainstem and increases activity immediately after sleep to drive arousal.

64
Q

How does the tuberomammillary nucleus influence wakefulness?

A

It releases histamine to promote arousal and alertness, with activity stopping during REM and non-REM sleep.

65
Q

Why do some antihistamines cause drowsiness?

A

They block histaminergic receptors, reducing wakefulness and promoting sleepiness.

66
Q

What is the role of the Raphe nuclei in regulating waking and sleeping?

A

-Release serotonergic outputs, promoting arousal and alertness.
- Their activity decreases during REM and non-REM sleep.

67
Q

How does loss of orexin neurons affect sleep?

A

Dysregulation of orexin neurons leads to rapid sleep onset, while loss of these neurons leads to hyperexcitability of REM-generating neurons, contributing to narcolepsy symptoms.

68
Q

Which brain structure inactivates the Ascending Arousal System (AAS), and how does it achieve this?

A

The ventral lateral preoptic nucleus (VLPO) inactivates the AAS by sending GABAergic projections that dampen arousal system activity, triggering the onset of sleep.

69
Q

What is the effect of lesions in the ventral lateral preoptic nucleus (VLPO)?

A

Loss of VLPO function induces insomnia due to the inability to suppress arousal systems.

70
Q

How do anesthetics interact with the VLPO and its role in sleep regulation?

A

Anesthetics enhance VLPO activity, mimicking natural sleep by inactivating the AAS and inducing brain wave patterns similar to REM sleep.

71
Q

How do benzodiazepines affect sleep architecture compared to placebo?

A

Benzodiazepines increase Stage II sleep while reducing deep slow-wave sleep (Stage III/IV) and REM sleep.

72
Q

What effect does caffeine have on sleep compared to placebo?

A

Delays sleep onset and reduces the duration of slow-wave sleep, leading to fragmented sleep patterns.

73
Q

In normal conditions (placebo), how is sleep structured across different stages over time?

A

Under placebo, sleep cycles alternate between REM and non-REM stages with progression into deeper slow-wave sleep early in the night.

74
Q

What changes occur in brain activity during sleep deprivation?

A

Reduces activity in the dorsal prefrontal cortex and dorsal striatum, while increasing activity in the medial temporal lobe (may explain heighened irritability)

75
Q

How do ampakines influence brain activity in sleep-deprived individuals?

A

Ampakines increase AMPA receptor activity, normalizing activity in the dorsal prefrontal cortex and reversing the under- and over-excitation caused by sleep deprivation.

76
Q

According to Freud, what role does the ego play in dreaming?

A

Freud suggested that during dreaming, the ego relaxes its control over the id, allowing unconscious thoughts to surface.

77
Q

What is the role of place cells and grid cells during awake behavior?

A

Place cells in the hippocampus and grid cells in the medial entorhinal cortex compute spatial navigation via reciprocal connections.

78
Q

How do hippocampal and entorhinal regions behave during rest compared to awake behavior?

A

During rest, hippocampal and entorhinal regions generate independent sequential activity, which helps strengthen and consolidate memories.

79
Q

During which sleep stage does somnambulism occur, and what characterizes it?

A
  • Occurs during stage 3 (non-REM) sleep
    -Characterized by impaired cognitive function and the absence of REM-related paralysis.
80
Q

What is REM Sleep Behavior Disorder (RBD), and what may cause it?

A
  • A condition where patients act out their dreams due to disrupted REM sleep.
  • May be caused by a synucleinopathy,that destroys brainstem neurons in the Ascending Arousal System (AAS).
81
Q

What brain waves occur during REM sleep?

A

Beta waves (high-frequency, active processing) and theta waves (lower-frequency, linked to dreaming and memory).