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Year 2 Brain and Behaviour > The Psychobiology of Depression and Mood (Michelle) > Flashcards

The Psychobiology of Depression and Mood (Michelle) Flashcards

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1
Q

How d we put clinical depression into perspective?

A
  • DSM-V criteria are more extreme than the typical fluctuations in mood that we all experience
  • Prolonged
  • Debilitating
  • Prohibit normal functioning
  • Not due to bereavement
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2
Q

What is the Stress-Diathesis model?

A
  • Model of depression
  • Diathesis means a genetic vulnerability to depression
  • Coupled with a stressor increases the likelihood of being diagnosed with depression
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3
Q

What are monoamines?

A
  • Family of neurotransmitters
  • Norepinephrine (NE: noradrenaline (NA))
  • Serotonin (5-HT)
  • Dopamine (DA)
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4
Q

What is the excitatory noradrenergic synapse pathway

A
  1. Production of NA
  2. NA release from vesicles at the synaptic cleft
  3. Activation of postsynaptic receptors
  4. Activation of autoreceptors
  5. Re-uptake unto presynaptic neuron
  6. Breakdown or storage
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5
Q

What does norepinephrine stimulate in the brain?

A
  • Mood
  • Attention
  • Motor control
  • Emotion
  • Energy
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6
Q

What does serotonin stimulate in the brain?

A
  • Mood
  • Anxiety
  • Appetite
  • Sleep
  • Sexual function
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7
Q

How do presynaptic autoreceptors work?

A
  • Neurotransmitter activates the receptor by binding to an extracellular site on the receptor
  • Neurotransmitter cannot enter the neuron through an autoreceptor
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8
Q

How do re-uptake sites work?

A
  • Neurotransmitter is transported back into the neuron
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9
Q

What are the effects or reserpine on monoamine synapses

A
  • Reserpine causes monoamines to leak out of vesicles
  • Monoamines are broken down by monoamine oxidase before it can cross the synapse
  • When the presynaptic neurone is activated there is no neurotransmitter available for release
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10
Q

What is the monoamine hypothesis of depression?

A
  • Major depression is due to a decrease in function of the monoamine system
  • Low levels of available 5-HT or NA
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11
Q

What is tryptophan?

A
  • Precursor of 5-HT

- Amino acid normally available in the diet

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12
Q

Tryptophan depletion study

Delgado et. al (1990)

A
  • Took depressed patients currently on medication and symptom free
  • Made them have a tryptophan-free diet for 2 days but also made them have a drink with a higher concentration of other amino acids e.g. protein
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13
Q

Tryptophan depletion study: Results

Delgado et. al (1990)

A
  • Due to competition across the blood brain barrier the other amino acids are taken into the brain resulting in low levels of tryptophan
  • Decrease in 5-HT
  • Symptoms of depression re-occurred
  • Once tryptophan was returned to the diet, symptoms went away
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14
Q

How do drugs work to increase 5-HT

A
  • Originally monoamine oxidase inhibitors which block the breakdown of 5-HT
  • 2nd and 3rd generation were re-uptake inhibitors which leaves more 5-HT in the synaptic gap
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15
Q

What is the time-lag effect of drugs?

A
  • All classes of antidepressant drugs increase 5-HT levels immediately (within hours)
  • Clinical response to drug treatment takes 3-5 weeks
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16
Q

What are the differences between NA and 5-HT neurons with chronic drug treatment?

A
  • Some re-uptake inhibitors act at NA synapses as well as serotonin synapses (SNRI)
  • For either system, autoreceptors become less responsive
  • For 5-HT: decrease in postsynaptic receptors, but they become more sensitive
  • For Noradrenalin: decrease in postsynaptic receptors and they become less sensitive
17
Q

What are the long term effects of drug treatment

A
  • Drugs like prozac rebalance the system
  • Restore 5-HT and NA levels to normal through adaptive processes in postsynaptic receptors
  • 5-HT receptors increase in sensitivity
  • NA receptors decrease in sensitivity
  • Both 5-HT and NA: downregulation
18
Q

What is the stress hypothesis of depression?

A
  • Chronic stress leads to depression
  • Because of increased HPA activity there is more cortisol in the body
  • Diminished negative feedback through loss of glucocorticoid receptors
19
Q

What is the role of CRH

A
  • Coordinates the stress response
  • Increases NA (locus ceruleus)
  • Released in limbic (emotional) brain regions
  • Injection of CRH increases fear and anxiety responses in animals
  • Too much CRH leads to imbalances noradranergic system, which puts the brake on 5-HT and reduces mood

Year 2 Brain and Behaviour (4 decks)

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