anxiety Flashcards
Noradrenaline in GAD
Systems are overactive - central and peripheral
Serotonin in GAD
Lack of SA:
- in BG (inadequately processing info)
- Cerebral Cortex (inadequately execute appropriate responses
-Limbic cortex/Amygdala (emotion/control of hypothalamus)
- helps silence neurons therefore lack of it means overactive brain
Noradrenaline in OCD
Less cerebellar and sympathetic outflow than GAD
Serotonin in OCD
Lack of SA:
- in BG/ thalamus (inadequately interpret/ processing info)
- Cerebral Cortex (less focused info from environment)
- Hippocampus (disturbances in memory processes
-Limbic cortex/Amygdala (emotion/control of hypothalamus)
- helps silence neurons therefore lack of it means overactive brain
- difference to GAD is hippocampus effect
Dopamine in OCD
increased DA function in basal ganglia, produces repetition of habits
* difference between OCD and GAD
Relationship between Hippocampus, Amygdala and Hypothalamus in PTSD
Hypo = regulates ANS (but doesnt in anxiety)
Hippo = meant to inhibt the hypo (but doesnt due to amygdala taking over) - shrinks overtime
amy = meant to activate hypo - grows in size, works harder in anxiety/ptsd
Two ways to silence the overactive brain
- increase negative charge into the neuron (Cl-)
- enhance inhibitory neurotransmission (IPSP), enhance GABA receptor activation to enhance Cl-
GABA receptor agonists (not very selective)
Barbiturates
More selective - GABA receptor agonists
benzodiazepines
negatives of barbiturates
high incidence of side effects, highly addictive
Benzos & GABA
benos enhance the effect of GABA on its receptor - have their own binding sites (Bz1,Bz2)
GABA-A receptor binds to what … to enhance…
bind both GABA and Benzos to enhance receptor function on the dendrite of the neuron
beta-adrenoreceptor antagonists are used for what ?
decrease noradrenaline to treat anxiety
Are drugs decreasing noradrenaline effective for anxiety?
only for peripheral effects (not really effective)
what receptor does Seratonin bind to
5-HT1A
what do the 5-HT receptors release into the neuron when serotonin binds
inhibitory G protein
what do Gi proteins do
create IPSP’s
what do SSRI’s do to increase IPSPs
block seratonin transporter that brings SA back into presynaptic terminal - keeps SA in terminal so it can bind to 5-HT1A receptors
what happens when seratonin stays in the synapse
the effect of serotonin lasts longer and more receptors are bound by it
reduced levels of SA in anxiety can be alleviated by SSRIs and what other way?
5HT1A-R agonist
what action do 5HT1A R agonists have?
act like serotonin and bind to 5-HT1A receptors
why do SSRI’s not work for inital 2 weeks
because 5-HT receptors are also on the presynaptic terminal that are more sensitive and so SA / 5HT agonists bind on them first (meaning they have less effect)
why do SSRIs take effect after the two weeks
presynaptic 5HT receptors are very sensitive so they hide (go back into the cell) if they are used too much
Role of cortisol in PTSD
Cortisol shrinks hippocampus w
