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Psychophysiology > Physiological Psychology Lecture #5 > Flashcards

Physiological Psychology Lecture #5 Flashcards

1
Q

Adenosine

A

Inhibitory.
1. Astrocytes store glycogen for “emergency energy”.

  1. Adenosine is by-product (ATP –> Adenosine)
  2. Accumulation of adenosine produces increase delta sleep.
  3. Adenosine increases steadily during day producing sleep feelings at night.
  • Caffeine blocks adenosine receptors
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2
Q

What does sleep deprivation lead to?

A

Decrease in glycogen stores and increase in adenosine which leads to sleepiness.

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3
Q

Histamines

A

Drugs that prevent synthesis of histamine cause decreased wakeful sensation and increase sleepiness.

  • Histamines activate the release of acetylcholine.
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4
Q

Acetylcholine

A

3 Groups of Ach Neurons:
- 1 in Hippocampus
- 2 located in the pons and forebrain

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5
Q

Cortical Desynchrony

A
  • Low voltage mixed frequencies.
  • Hallmark of REM sleep
  • Contributes to belief that REM sleep may play an important role in facilitating synaptic plasticity of recently acquiring memory traces.
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6
Q

Serotonin

A
  • Play a role in activation behavior.
  • Low during REM sleep = limited movement.
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7
Q

Norepinephrine

A

Produces arousal and sleeplessness.
- Mediated by the locus coeruleus in the pons.
- Increase locus coeruleus firing = increase vigilance/focus

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8
Q

Orexin

A
  • Secreted by hypothalamus
  • Stimulates other neurons to promote alertness and energy metabolism in response to stress in the environment.
  • High during alert or active waking, especially exploratory activity.
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9
Q

Melatonin

A
  • Produced by the pineal gland in response to evening/darkness about 2 hours before normal sleep time.
  • Serotonin is converted into melatonin.
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10
Q

Insomnia

A
  • Effects 30% of adults.
  • 40% of women, 30% of men
  • High comorbidity rate with chronic medical conditions.
  • Chronic use of sleep-promoting drugs can cause rebound insomnia.
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11
Q

Primary Insomnia

A

Difficulty falling asleep after going to bed or after awakening during the night.

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12
Q

Secondary Insomnia

A

Inability to sleep due to another mental or physical condition.

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13
Q

Narcolepsy

A
  • Orexin-Related Neurological d/o
  • REM related symptoms occur inappropriately.
  • > 85% orexin producing neurons.
  • Hereditary component.
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14
Q

Sleep Attacks

A

Overwhelming urge to sleep.
- Triggered under boring and monotonous conditions.
- Lasts 2-5 minutes
- Wake up refreshed

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15
Q

Cataplexy

A

Sudden muscle weakness/paralysis.
- Triggered by strong emotional reaction to physical exertion.
- Remain fully conscious.
- Loss of muscle control due to massive inhibition of motor neurons in spinal cord.

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16
Q

Sleep Paralysis

A

Inability to move before onset of sleep or waking.

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17
Q

Narcolepsy Treatment

A

Modafinil, methylphenidate, SSRIs

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18
Q

REM Sleep Behavior Disorder

A

Lack of muscle paralysis during REM can lead to acting out dreams.
- Can be comorbid with narcolepsy.
- Typical onset 60+ years
- Believed to be neurodegenerative.

Treatment: Clonazepam.

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19
Q

Sleep Apnea

A

Difficulties sleeping and breathing at the same time.
- Wake up gasping for air and decrease slow wave activity.

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20
Q

Obstructive Sleep Apnea

A

Due to narrowing of airway (obesity, enlarged tonsils, hormonal changes)

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21
Q

Central Sleep Apnea

A

Brain does not signal need to breath.

22
Q

Untreated Sleep Apnea

A
  • Significant deficits in attention, memory, and executive functions.
  • In kids, 2.5x risk of behavioral problems.
23
Q

How is sleep apnea treated?

A

Treated vis CPAP, BiPAP

24
Q

Alzheimer’s Disease

A

Disordered Cardiac Rhythm
- Body temperature lowers between 9-noon (rather than 4-5am)

25
Q

Schizophrenia

A

Disordered Cardiac Rhythm
- Melatonin production lages (2-3am)
- Rhythms collapse in some patients.
- Pattern can persist despite improvement of sleep quality and quality with antipsychotic agents.
- Treatment with Ramelteon improved sleep w/o negative benzo side effects.

26
Q

Depression

A

40-60% report sleep problems.

27
Q

Suicide

A

Sleep deprivation independent risk factor.

28
Q

Sleep D/O Post-TBI

A
  • Up to 80% report sleep problems after injury.
  • Female sex, Black race, history of TBI, and psychiatric history were all associated with severe persistent insomnia.
  • Poor sleep = poorer recovery trajectory due to increased risk for mood d/os, ongoing cognitive deficits, and neurodegeneration.
29
Q

Sleep and Learning

A
  • All-nighter can cause up to 40% decrease in brain activity.
  • Taking a nap following studying and class–consolidation of learning.
30
Q

Jame’s Lange Theory of Emotion

A

Stimulis –> Physiological Arousal –> Emotional Response

31
Q

Cannon-Bard Theory of Emotion

A

Stimulus –> emotional response/physiological arousal

32
Q

Scachter-Singer Theory

A

Stimulus –> Phsyiological Arousal –> Cognitive Appraisal –> Emotional Response

33
Q

Fear

A

Amygdala–core processor of conscious and unconscious fear and value.
- Plays a key role in learning conditioned responses towards aversive stimuli.

34
Q

Episodic Memory

A

Long term memory that involves conscious recollection of previous experiences.

35
Q

Long Term Potentiation

A

Process involving persistent strengthening synapses that leads to a long-last increase in signal transmission between neurons.

36
Q

W/ Hippocampus –>

A

Long-term memories

37
Q

W/ Hypothalamus –>

A

Sympathetic Nervous Response (fight or flight)

38
Q

W/ Thalamus –>

A

Unconscious Fear Processing

39
Q

Lateral Nucleus

A

Inside Amygdala
- Regarded as sensory input gateway.
- Located in dorso-lateral part of the Amygdala.

40
Q

Central Nucleus

A

Key role in emotional response to aversive stimuli –> Stress
- Damage = decrease in stress hormones, ulcers, and stress-induced illnesses.
- Stimulation = increased fear, agitation, gastric ulcers.

41
Q

Basal Nucleus

A

Major output pathways to cerebral cortex.
- Projects to the VMPFC which leads to extinction of the conditioned fear.
- In PTSD, increased amygdala and decrease VMPFC activation.

42
Q

Kluver-Bucy Syndrome

A

Can be cause by stroke, encephalitis, tumors, TBI and even a lobotomy.
- Damage to the bilateral amygdaloid nuclei and hippocampus.

  • Results in:
    Absence of fear and anger response
    Psychic blindness/visual agnosia
    Hyper-orality
    Hyper-Sexuality w/o sexual desire
    Binge eating disorder
    Memory disorders
43
Q

Ubach-Weithe Disease

A

Rare genetic disorder.
- Progressive damaging to neural tissue.
- First symptoms: weak cry/hoarse voice.
- Absence of startle or fear response.

44
Q

Aggression

A

50-65% heritability.
- Serotonins inhibit aggressions and risky behaviors.

45
Q

Testosterone’s impact on aggression

A

Increase in testosterone = increase in prosociability.
- Increase amygdala, hypothalamus, and PAG activation only if shown angry faces or given an unfair deal.
- Testosterone only increased aggression in those with high dominance traits.

46
Q

VMPFC

A

The VMPFC plays a role in Impulse Control, Courage, Moral-Decision Making.
Reduced activation/volume of the VMPFC is seen in in individuals with antisocial personality disorder and impulsive/emotional murderers.

47
Q

Love and the Brain

A
  • Photos of romantic partner increase caudate nucleus (processes visual information) and increase ventral tegmental area (mediates reward system).
  • Increase cortisol and adrenalin.
48
Q

Post Orgasm

A

Women: increase oxytocin
Men: increase vasopressin

49
Q

Orbitofrontal Cortex

A
  • Involved in emotional expression.
  • Gets information from frontal lobe, sensory system, and amygdala.
50
Q

Affective Blindness

A

Those with damage to the visual cortex, can recognize facial expressions of emotions w/o conscious awareness of looking at a person’s face.

Psychophysiology (11 decks)

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