T3L8 anxiety neurobiology

Question 1

amygdala and fear

Answer 1

• divisions and connections within involved with emotion

- lesions can stop fear of specific things: eg unilateral amygdala removal stops spider phobia

Question 2

stress response

Answer 2

• from fearful stimuli
• depends on HPA axis - hypothalamus, pituitary and adrenal cortex

hypothalamus releases CRH
pituitary releases ACTH
adrenal releases cortisol (stress hormone)

locus coeruleus releases noradrenaline
- fight or flight

Question 3

push pull regulation of HPA axis

Answer 3

s8

hippocampus gives -ve feedback to reduce cortisol

amygdala makes you stressed

Question 4

chronic stress

Answer 4

activation of glucocorticoid receptors in hippocampus

• increase Ca2+ entry into neurons
• increase Ca2+ > excitotoxic> cell death

as hippocampus cant limit cortisol production

anxiety may result from:

• diminished hippocampal activity
• loss of amygdala feedback
• inappropriate fear
• hippocampal size decrease in ptsd

Question 5

hm

Answer 5

both hippocampus and amygdala have access to highly processed info from other brain areas
- eg diffuse modulatory systems
- noradrenergic system
- serotonergic system
(the 2 balance each other)

Question 6

panic disorder

Answer 6

Characterized by unrealistic, unfounded fear and anxiety; acute and unremitting terror for variable lengths of time

treated with benzos- agonise GABAa receptor eg diazepam

or SSRI

or cognitive therapy

• noradrenaline makes you alert
• serotonin inhibits noradrenaline
  opposing functions (eg in amygdala, hippocampus)
• shifted balance between these 2 linked to panic disorder- fear response to inappropriate stimuli

SSRIs increase 5HT response, inhibit noradrenaline, push balance back

Question 7

benzos work for

Answer 7

• GAD generalised anxiety disorder
• panic

not for:

• OCD
• PTSD

Question 8

SSRIs work for

Answer 8

• OCD
• PTSD
• PD
• GAD

Question 9

Busprirone works for

Answer 9

GAD

6-HT receptor partial agonist

Question 10

serotonergic system and anxiety

Answer 10

SSRIs

buspirone
5HT partial agonist

action of SSRIs is to do with receptors rather than gap junction so effects take a week or so to come on

its the adaptive changes of ns to chronically high serotonin levels

cascade of serotonin can lead to changes in plasticity and morphology of neurons
- this could aid reversal of stress induced changes may restore normal function to brain
s22

Question 11

OCD

Answer 11

Frequently recurring, uncontrollable, anxiety-producing thoughts (obsessions) and impulses (compulsions). Responding to them, e.g. repeated, compulsive hand washing, dissipates associated anxiety

• patients recognise that their thought and behaviours are irrational
• 1-2%
• genetic (common underlying genotype for OCD and Tourette’s)
• environmental - eg stressful life events, strep infection
• imbalance of direct and indirect pathways

theory 1:

• the direct pathway is previously learned behavioural sequences- they can be automatic and rapidly executed
• the indirect pathway suppresses these automatic behaviours, allowing the person switch to adaptive behaviours
• overactivity of direct pathway means the indirect pathway cannot switch it off

theory 2:

• caudate sends inhibitory projections to globus pallidus which sends inhibition to thalamus which projects to orbitofrontal cortex
• OCD may be disinhibition leading to reverberation in this circuit
• treat with SSRI (delayed onset), benzos (immediate)