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PSYBIO > L5: Neurotransmission: Anxiety > Flashcards

L5: Neurotransmission: Anxiety Flashcards

1
Q

What is the difference between anxiety and clinical anxiety?

A

Anxiety = feelings of fear with no reasonable external cause

Clinical Anxiety = same + interferes with other activities and prioirities

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2
Q

What are the 2 main symptoms of clinical anxiety?

A
  1. Fear

2. Worry

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3
Q

How does fear manifest in someone with clinical anxiety?

A
  • panic

- phobia

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4
Q

How does worry manifest in someone with clinical anxiety?

A
  • Anxious misery
  • apprehensive
  • expectation
  • obsessions
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5
Q

What is the typical treatment given to someone with clinical anxiety?

A

NICE - mostly based around behavioural treatments

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6
Q

Give in order the ‘history’ of drugs used to tackle clinical anxiety

A
  1. Barbiturates: mephobarbital
  2. Benzodiazepines: Valium
  3. SSRI - selective serotonin re-uptake inhibitors
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7
Q

Why are barbiturates no longer used to treat clinical anxiety since 1960’s?

A

initially thought to be good as it is an effective anxiolytic BUT….

  • has low therapeutic index = easy to over dose
  • acts in a relatively non-specific way
  • induce tolerance + dependence
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8
Q

Why are benzodiazepine preferred over barbiturates?

A

Ben has…

  • higher therapeutic index = safer to overdose
  • SPECIFIC anxiolytic effect
  • used for a range of clinical disorders
  • initially thought to not induce dependence but now a major issue in their use
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9
Q

Which of the three drugs, barbiturates, benzodiazepine and SSRI, are the first in line for pharmacological treatment for many anxiety disorders?

A

SSRI
- used in GAD
- do have a delayed onset of action
(NICE guidelines, 2011)

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10
Q

Regarding the 2 different models to treating pathology, disease or symptom -centred, what are we hoping to achieve with the use of drugs?

A

Disease-centred
- suggests drugs restore normal function of the brain

Symptom-centred

  • suggests drugs produce specific changes in aspects of mood
  • no necessary assumption drugs will reverse some pre-existing neurochemical abnormality
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11
Q

Which neurotransmitter system does benzodiazepine selectively act on?

A

GABA

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12
Q

Describe the basic transference of information on the GABA neurotransmitter system

A
  1. GABA within vesicles in the pre-synaptic terminal
  2. Depolarisation results in the release of GABA
    - this will act on GABA receptors on the post-synaptic receptors
  3. Then GABA is transported back into pre-synaptic terms/ adjacent glial cells by the re-uptake pump
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13
Q

What are the 2 ways in which a neurotransmitter system can be inactivated?

A
  • re-uptake

- breakdown

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14
Q

What is a receptor constructed from?

A

a series of subunits - proteins

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15
Q

What happens when benzodiazepine binds to GABA-A receptors?

A

Enhances the effect of GABA

  • opens a pore in the GABA-A receptor
  • allows Cl- to enter (down concentration gradient = keep cell negative)
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16
Q

Other than benzodiazepine, what other drug can bind to the GABA-A receptor?

A
  • Alcohol

- Barbiturates

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17
Q

Briefly describe how an AP is induced?

A
  1. NA+ enters - in response to mild depolarisation
    - causes axon to depolarise
    = AP as more positive (-55V)
  2. K+ leaves
    - action repolarises (-70)
  3. Brief hyperpolarising = refractory period
18
Q

How does GABA effect AP?

A

Inhibitory effect:
- GABA = increases Cl- entering cell = -65mv
- meaning the inside remains more negative so cannot reach the -55V threshold for AP
= GABA impedes depolarisation = making an AP less likely

19
Q

What is the difference in effect when Benzodiazepine binds to just GABA or to GABA-A?

A

GABA = little enhancement of the GABA effect

GABA-A = greater enhancement of the GABA effect

20
Q

what behaviour effect would you expect if you developed a drug which reduced the effect of GABA at the GABA-A receptor?

A

Behavioural:

  • hoped for increased alertness/ cognitive enhancers
  • Got: lots of fear sensations

Useful?
- military: enhanced interrogation technique

21
Q

Describe the GABA-A receptors

A

Made up of 5 separate subunits

  • each is a protein
  • coded by a different gene

Subunits are slightly variable in their structure
- altering the sensitivity of the receptor to benzodiazepines

22
Q

In what parts of the brain are benzodiazepine-sensitive GABA-A receptors found?

A

mouse brain:
- White + yellow = highest densities

= hippocampus
= amygdala

= + related structures

23
Q

What are the 2 major classes of GABA receptor subtypes and their differences?

A
  1. GABA-A receptors
    - ionotropic receptor (membrane bound)
    - composed of 5 units
    - Considerable variety in the detailed sub-unit structures
  2. GABA-B receptors
    - metabotropic receptor (acts through second messenger)
    - works more slowly in a more sustained way
24
Q

What evidence is there suggesting the amygdala is involved in fear - conditioning?

A
  1. Rats conditioned to fear a tone after pairing tone and foot shock
  2. Tone alone = increase in blood pressure + freezing
  3. Conditioning process greatly reduced when the amygdala in rats was damaged
25
Q

What evidence is there suggesting the amygdala plays a role in processing linguistically coded threat stimuli?

A
  1. ppt asked to name colours of words that are either related to persecution, threat of destruction
  2. Fear-relevant words produced greater activation of amygdala (deep within the temporal lobe)
26
Q

What is referred to by the term ‘neural circuit of fear’?

A
  • the different parts of the brain affected by the output of the amygdala producing the different aspects of fear
  1. Autonomic symptoms
    - blood pressure
    - heart change
  2. Hormonal changes
    - increased adrenaline, cortisol
  3. Processing of fear-related stimuli
27
Q

What is noradrenaline?

A
  • peripheral stress hormone

- central neurotransmitter

28
Q

What does the Locus coeruleus (hindbrain) contain?

A
  • noradrenergic cell bodies

- sub-cortical structures including amygdala

29
Q

How have noradrenaline been linked to modulating amygdala fear circuits?

A

LC contains noradrenergic cell bodies

  • selective chemogenetic stimulation of these neurons delays the extinction of a simple fear response in rats
    • effect is blocked by propranolol (noradrenergic beta receptor antagonist)
  • relevant for PTSD?
30
Q

Why is it suggested benzodiazepines may modulate GABA-ergic inputs to amygdala?

A

There are many other otential modulators of amygdala function (Serotonin (5HT))
- GABA being one of them and benzo works on GABA

31
Q

Through which circuit are fear and worry related sympomts thought to be produced by?

A

Fear = amygdala-centred circuit

Worry = Cortico-striato-thalamo-cortical circuit (CSTC)

32
Q

Which loops from the Dorsolateral prefrontal cortex (DLPFC) is thought to be especially important in worry and anxiety?

A

(CSTC) cortico-Striatum + thamalus loops

  • responsible for modulation of motor output + cognition
33
Q

Why is benzo suggested to modulate GABA-ergic inputs to the CSTC ‘worry loop’?

A

One of the many drugs which can bind to the CSTC area including

  • 5HT
  • Glutamate
34
Q

What major overlaps do depression and anxiety have?

A
  1. Sleep
  2. Concentration
  3. Fatigue
  4. Psychomotor
35
Q

What may the overlap between MDD and GAD suggest about drugs used to treat them?

A
  • may be some overlap in drugs that are effective in treating anxiety and depression
36
Q

What are some non-benzodiazepine anxiolytics?

A
  1. SSRIs
  2. Buspirone
  3. VSCCs - modulators of Voltage Sensitive Calcium channels
  4. Noradrenergic antagonists
37
Q

How do SSRI act as anxiolytics?

A
  • enhance serotonergic inhibition in both amygdala + CSTC related circuits
  • widely prescribed for depression
38
Q

How does Buspirone act as an anxiolytic?

A
  • serotonergic drug

- different mechanism of action compared to SSRI but achieve a broadly similar effect

39
Q

How do VSCCs act as anxiolytics?

A

Modulators of Voltage Sensitive Calcium channels

  • may reduce excitatory glutamate transmission in amygdala + CSTC related circuits
  • EG: gabapentin, pregabalin
40
Q

How do noradrenergic antagonists act as anxiolytics?

A
  • drug binds to site causing no effect
  • May reduce noradrenergic inputs that normally enhance vigilance
    • partly via effect on hippo + amygdala
  • can also reduce autonomic components of anxiety = shaking

PSYBIO (5 decks)

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