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Biological Psychology > Stress and Mood Disorders > Flashcards

Stress and Mood Disorders Flashcards

1
Q

What does the stress response do?

A
  1. Mobilise energy stores
  2. Increase blood flow to brain and muscles
  3. Decrease blood flow to digestive and reproductive systems
  4. No energy wasted on growth, reproduction, and healing
  5. Ignore pain
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2
Q

Metabolic Stress response

A

Insulin is suppressed but glucagon is released. This causes the release of glucose and energy

Catecholomines and glucocorticoids are also released.

Long term response is weakness and fatigue

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3
Q

Suppression of the HPA axis - Feedback of cortisol on the PVN

A
  1. Cortisol binds to glucocorticoid receptors
  2. This triggers release of endocannabinoids
  3. These inhibit release of glutamate from pre-synaptic terminals onto PVN
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4
Q

Suppression of the HPA axis - Hippocampus

A
  1. Indirect inhibition
  2. Contains many mineralocorticoid receptors
  3. Intermediate-term feedback: returns psychogenic stress response back to baseline
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5
Q

Pituitary Gland

A

Beta-endorphins is released from the pituitary gland as a hormone to suppress pain. Also releases vasopressin

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6
Q

Cardio-vascular stress response

A

Vasopressin recovers more water in the kidneys leading to an increase in blood volume.

Sympathetic nervous system causes increased heart rate and vasoconstriction, which in turn increases blood pressure.

Long term leads to coronary heart disease

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7
Q

Major Depression symptoms

A
  1. Depressed mood
  2. Sleeping problems
  3. Fatigue
  4. Change in appetite
  5. Lethargy
  6. Feelings of worthlessness
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8
Q

Depression and the HPA axis

A

Dysregulated HPA axis is common in affective disorders

Both pathological increases and decreases in cortisol can lead to depressive symptoms

Chronic stress is a major risk factor for depression

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9
Q

Chronic Stress

A

Amygdala –> HPA Axis –> cortisol

Glucocorticoids (cortisol) –> Locus Coeruleus –> noradrenergic projections –> amygdala

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10
Q

How do glucocorticoids damage the hippocampus?

A

They reduce adult hippocampal neurogenesis and shrink dendritic arbors. They also reduce glucose uptake and in the long run kill hippocampal neurons.

All this leads to smaller hippocampal volume

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11
Q

Other effects of chronic stress

A
  1. Depletion of noradrenaline from locus coeruleus
  2. Depletion of serotonin from Raphe Nuclei
  3. Depletion of dopamine from Ventral Tegmental Area to nucleus acumen and prefrontal cortex
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12
Q

Sleep in Major Depressive Disorder

A

Shorter REM and short sleep latency (fall asleep straight away).

Can be caused by some anti-depressants that suppress REM sleep.

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13
Q

Lowering mood with sleep

A

Phase shift between endogenous circadian rhythm and externally imposed sleep-wake cycle can lead to lower mood/depression

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14
Q

Depression and circadian cycle

A

Circadian cycle is often advanced with depressed patients. Going to sleep with circadian clock, then slowly shifting the clock may help with depression.

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15
Q

Bright Light Treatment

A

Seems to have positive effects for non-seasonal depression. Could be related to the advanced circadian clock.

Evidence of connection between melanopsin-containing RGCs and vIPOA

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16
Q

What mono-amine induces depression?

A

Reserpine (mono-amine antagonist) induces depression

Lower levels of 5-HIAA (what is made by serotonin) in cerebrospinal Fluid also induces.

Same with tryptophan.

17
Q

SSRIs

A

Usually ingested through pills
Very lipophilic
Different pharmacokinetics for different drugs: (Prozac - slow uptake, half life of 1-4 days; Faverin - bit faster, half-life 8-28 hours; Cipramil: bit faster, half life of around 36 hours)

18
Q

Negatives of SSRIs

A

SSRIs only work after several weeks as the first 2 weeks use an adaption of auto receptors.

In further weeks they could have the opposite effect and normalise HPA axis feedback

19
Q

Adult hippocampal neurogenesis

A

Anti-depressants increase neurogenesis
Time course of increase = time course of effectiveness
Destroying adult neurogenesis prevents anti-depressant effects
Exercise increases adult neurogenesis and improves depression symptoms

20
Q

Other uses of SSRIs

A
  1. Anxiety Disorders
  2. Panic Disorder
  3. OCD
  4. Eating Disorders
21
Q

Ketamine

A

Dissociative anaesthetic and analgesic
Taken as a snorted powder, in pills, or injected
Half-life of 10-15 minutes and lasts 45 minutes

22
Q

Short term effects of low doses of ketamine

A

Lightness and euphoria
Disconnection of thoughts and from the world
Strange perceptions

23
Q

Short term effects of high doses of ketamine

A

Mind-body disconnect and K-holing (unresponsive to the world and having hallucinations)

24
Q

Ketamine physiological action

A

NMDA-R Antagonist

Responsible for anaesthesia, dissociation and hallucinations, amnesia and analgesia (in the spinal cord)

25
Q

Ketamine as an antidepressant

A

Sub-anaesthetic dose can have a profound effect on depression within hours of injection.
Typically a course of several doses per week for a few weeks
Does not last more than a few months

26
Q

Why does ketamine help limit depression?

A

Seems to work through new synapse formation in anterior cingulate cortex

27
Q

Ketamine long term effects

A

Memory/cognitive problems (possibly reversible)
Bladder and kidney damage (irreversible)
Abdominal cramps (k-cramps)

28
Q

Ketamine physical addictiveness

A

Tolerance does build up

Withdrawal symptoms include psychotic features

29
Q

Ketamine psychological addictiveness

A

Less known about it but NMDA-R antagonists can influence dopamine release in n-Acc

30
Q

Anxiety disorders

A

A range of disorders, characterised by extreme worry, fear and chronic stress.
Often comorbid with depression and other disorders
To be a disorder it has to last more than 6 months, be inappropriate to the situation, and be debilitating
Twice as common in women than men

31
Q

Treatments for anxiety

A
  1. Talking therapy like CBT
  2. Exposure therapies
  3. Drug treatments (SSRIs, beta-blockers, benzodiazepines)
32
Q

Benzodiazepines: Sedatives and Anxiolytics

A

Usually ingested
Reach maximum blood concentration in about an hour
Lipid solubility varies from drug to drug
Depending on the exact chemical, half-life can be 90 minutes-6 days.

33
Q

Benzodiazepines short term effects

A 
Sleepiness
Reduction of anxiety
Anterograde amnesia
Muscle relaxation
Mental confusion
Overdose can be lethal if taken with alcohol
34
Q

Benzodiazepines Physiological Action

A

Facilitation of GABA-A receptors (increases inhibitory processes)

35
Q

Benzodiazepines Short Term effects - Clinical use

A

Sleeping pills against insomnia
Anxiolytic against anxiety and panic disorders
Recovery from alcohol withdrawal
Anticonvulsant in combination with other drugs

36
Q

Benzodiazepines long term effects

A

Mental confusion
Induction or extension of dementia
Learning problems
Can improve after medication stops

37
Q

Benzodiazepines Addictiveness - Physical

A

Will develop even with therapeutic doses

Withdrawal symptoms include anxiety, insomnia, restlessness, agitation, and irritability

38
Q

Benzodiazepines Addictiveness - Psychological

A

Alcoholics can be sensitive to benzodiazepine addiction as well
There are GABA-A receptors in the Ventral Tegmental area and the N Accumbens.

Biological Psychology (7 decks)

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