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Neuropsychopharmacology > Week 3 - Anxiety > Flashcards

Week 3 - Anxiety Flashcards

1
Q

Anxiety=

A

reactions due to anticipation of negative event

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2
Q

What are the four main brain areas involved in anxiety?

A

Amygdala, hippocampus hypothalamus and the locus coeruleus

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3
Q

What are the two main responses to threat? Explain a little about what they do

A

Immediate (subcortical) response to threat:
- You receive visual and auditory stimuli. The amygdala alerts other brain structures, surges in cortisol and noradrenaline prepared for fight or flight response.

Cognitive processing of immediate response to threat:
- The cortex and basal ganglia decide whether to continue or discontinue the fear response.
- If it is decided to maintain the fear response, the amygdala remains on the alert

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4
Q

Depression and anxiety are not comorbid

A

False - they are highly comorbid

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5
Q

GAD definition:

A

Excessive on-going anxiety without reason or focus. Overactivity of the sympathetic nervous system

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6
Q

What neurotransmitters are involved in GAD?

A
  • > noradrenaline
  • < serotonin
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7
Q

What receptor does serotonin usually inhibit, that is overactive in GAD?

A

5-HT1A

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8
Q

What brain regions exhibit increased activity in GAD as a result of serotonin deficiency?

A
  • Cerebral cortex
  • Basal ganglia
  • Limbic cortex/Amygdala
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9
Q

What brain regions exhibit increased activity in OCD as a result of serotonin deficiency?

A
  • Cerebral cortex,
  • Basal ganglia/Thalamus,
  • Limbic cortex/Amygdala
  • Hippocampus
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10
Q

What brain areas are involved in OCD and what is the proposed cause?

A

May be caused by uncontrolled communication (loop) between frontal, striatal and thalamic structures

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11
Q

What neurotransmitters are involved in OCD?

A
  • > noradrenaline
  • < serotonin
  • > dopamine
    (nigrostriatal)
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12
Q

What is the HPA axis and what is it involved in?

A

Involves the Hypothalamus, Pituitary Gland and Amygdala.

Involved in release of cortisol

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13
Q

What is the role of the hippocampus and the amygdala is PTSD?

A

The hippocampus is supposed to suppress the hypothalamus however because the ratio between the amygdala and the hippocampus is increased, the Amygdala dominates.

This leads to the release of cortisol and the activation of the autonomic nervous system.

(PFC also quells amygdala
PTSD also loss of PFC control)

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14
Q

What do people who don’t develop PTSD have in common in the brain?

A

They haven’t lost control of the PFC so therefore the PFC can calm the amygdala

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15
Q

What can you have in PTSD abnormal ____ or abnormal ____?

A

Cortisol or noradrenaline

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16
Q

Which part of the brain is bigger in PTSD?

A

The amygdala is bigger (dominates over) the hippocampus

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17
Q

How can we reduce (over) activity of neurons?

A

Enhance inhibitory neurotransmission (IPSP)
- enhance GABA receptor activation to enhance Cl-

18
Q

What were early treatments of anxiety?

A

Early treatments consisted of using barbiturates
- Act as GABA Receptor agonists - not very selective

Overtaken by the benzodiazepines
- More selective as GABA receptor agonists

19
Q

What do benzodiazepines do?

A

Reduce anxiety and aggression

Benzodiazepines enhance the effect of GABA on it’s receptor. They have their own binding site on the GABA A receptors: Bz1 and Bz2.

This keeps the channel open for longer which lets the chloride ions into the cell = inhibit neurons such as dopamine or noradrenaline.

20
Q

What are anxiety treatment shifting towards?

A

Shifting from the ‘global’
treatment with benzodiazepines to more specific treatments.
- Specifically decrease noradrenaline (only beneficial for peripheral effects)
- Specifically increase serotonin

21
Q

What is specifically decreasing noradrenaline useful for?

A

Only beneficial for peripheral effects. e.g. if you have a presentation you can take a beta blocker to just get you through the presentation

However overtime it isn’t good long term.

22
Q

Is specifically decreasing noradrenaline helpful in the long term?

A

NO

23
Q

Why are barbiturates and benzos not preferred?

A

They target the system globally rather than specific neurons/ parts of the brain. They are sedating.

24
Q

What overtook barbiturates but have a similar mechanism? and why?

A

Benzos because they have fewer bad side effects, aren’t as lethal and aren’t as addictive.

25
Q

SERT=

A

Serotonin transporter

26
Q

Small IPSP =

A

not likely to influence overall activity of neuron

27
Q

Effect of SSRI’s =

A

Serotonin Transporter
is blocked by SSRI.
The effect of serotonin
lasts longer in the synapse & more receptors (5-HT1A)
are bound by 5-HT.

28
Q

Gi=

A

inhibitory G-protein

29
Q

What is the main catch of SSRIs?

A

They take 2-3 weeks to work

30
Q

Why do SSRIs take 2-3 weeks to work?

A

It takes time for the 5HT1-A receptors that are presynaptic to remove themselves and go back inside the cell. They desensitise/hide if they get stimulated too much and go inside the cell to hide.

31
Q

What are the main treatments of anxiety?

A

Barbiturates (not used)

Benzodiazapine (global)

SSRIs (agonist)

Serotonin 5-HT1A receptor agonists

32
Q

Where to barbiturates bind?

A

Gabba

33
Q

Where to benzos bind?

A

Gabba (but they have their on binding site) - they let more chlorides in to the cell = more IPSPs = calm down monoamines

34
Q

What is used to treat Mania? (generally)

A

Mood stabilizers are used to treat mania

35
Q

List the treatments for mania?

A

Lithium carbonate (salts)

Anticonvulsants

Neuroleptics (often prescribed with Lithium or Anticonvulsants)

36
Q

What is the mechanism of action for lithium salts?

A

Stabilize neurons by reducing the ability
of receptors to communicate with second messenger systems

Second messengers are BLOCKED = EPSP is not produced

37
Q

Downside of lithium salts?

A

Lithium Salts Have Many Side Effects

38
Q

What is the mechanism of action of Anticonvulsants?

A

Inhibiting sodium and calcium channels from working helps to
reduce the firing of the neurons (stops overactivity of monoamines)

Also inhibit second messenger systems (similar to lithium salts) - stops EPSPs

39
Q

What ions do Anticonvulsants stop coming in?

A

Calcium and sodium

40
Q

What is Electroconvulsive Therapy (ECT)

A

A form of mood stabilisation where you pass electricity through the temporal lobes

Neuropsychopharmacology (8 decks)

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