5- Neurotransmission Flashcards

1
Q

What is anxiety

A

A feeling of fear or dread when there is no ‘reasonable’ external cause for anxiety, and fear otherwise.

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2
Q

Clinical anxiety refers to

A

Anxiety which is ‘pathological’, interfering with other activities and priorities.

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3
Q

Symptoms of anxiety

A
  • Phobia
  • Panic
  • Anxious misery
  • Apprehensive expectation
  • Obsessions
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4
Q

Drug Treatment of Anxiety

A
  • Barbiturates
  • Benzodiazepines
  • Selective serotonin reuptake inhibitors
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5
Q

Selective serotonin reuptake inhibitors

A
  • First line pharmacological treatment (NICE guidelines 2011)
  • Used for general Anxiety disorder (GAD)
  • They do have a delayed onset of action.
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6
Q

Benzodiazepines

A
  • Evidence for a specific anxiolytic effect
  • They are substantially safer than barbiturates in overdose
  • Used for a number of other clinical conditions
  • Initially thought not to induce dependence however there seems to be an issue
  • e.g. Valium
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7
Q

Barbiturates

A
  • have a low therapeutic index
  • Act in a relatively non-specific way
  • Induce tolerance and dependence
  • Clinical use for anxiety ceased in the 1960’s.
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8
Q

A ‘disease-centred’ model for anxiety believes

A

A drug restores the brain to normal function

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9
Q

A ‘symptom-centred’ model for anxiety believes

A

Drugs produce specific changes in aspects of mood, motivation and cognition that make a condition, such as clinical anxiety, less disabling
No assumption drugs ‘reverse’ brain to normal

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10
Q

Depolarisation will lead to

A

GABA release, which will act at the postsynaptic GABA receptors and then be transported back into the presynaptic terminal

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11
Q

What do benzodiazepines do

A

Enhances the effect of GABA but has ‘no’ effect by itself.

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12
Q

The alpha GABA receptor also has (separate) binding sites for

A

Alcohol and barbiturates

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13
Q

How many subunits in the alpha GABA receptors are there

A

5 separate subunits - each is a protein and coded by a different gene

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14
Q

Benzodiazepine-sensitive alpha GABA receptors are selectively expressed higher in which brain areas

A

The hippocampus, amygdala and related structures.

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15
Q

Two major classes of GABA receptor subtypes

A
  • Alpha GABA (GABAA)

- Beta GABA (GABAB), a metabotrophic receptor – G-protein coupled

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16
Q

Fear-relevant words produce greater activation of

A

Amygdala

17
Q

Outputs from the amygdala can modulate different aspects of fear including

A
  • Autonomic symptoms
  • Hormonal changes
  • Processing of fear-related stimuli
18
Q

How do those with damage to the amygdala react to fear

A

Their experience of fear and panic was as great as in the controls who also experienced a panic attack

19
Q

Complex neural loops run between cortex, striatum and thalamus (CSTC loops) and are responsible for

A

Modulation of motor output and cognition

20
Q

Which loop may be responsible for worry and anxiety

A

Dorsolateral prefrontal cortex (DLFPC)

21
Q

There is overlap between GAD and

A

Major depressive disorder (MDD)

22
Q

Selective serotonin reuptake inhibitors (SSRIs) will enhance

A

Serotonergic inhibition in both amygala- and CSTC related circuits

23
Q

Noradrenergic antagonists may reduce noradrenergic inputs which

A

Can reduce autonomic components of anxiety

24
Q

Selective serotonin reuptake inhibitors do what

A

Slow the the removal of serotonin from the synaptic cleft

25
Q

Buspirone acts as a partial agonist at

A

Some types of serotonin receptor

26
Q

Noradrenaline is both

A
  • A peripheral stress hormone

- A central neurotransmitter.

27
Q

The locus coeruleus (hindbrain) contains

A
  • noradrenergic cell bodies that project forwards to cortex

- Sub-cortical structures including the amygdala.

28
Q

Selective chemogenetic stimulation of noradrenergic cell bodies does what

A

Delays the extinction of a simple fear response in rats

29
Q

What is propranolol

A

A noradrenergic beta receptor antagonist.