Lect 4 Flashcards
note that cary seemed to integrate the HPA theory with the one about BDNF versus the textbook seems to present them as seperate things
see slides
describe the HPA axis and its disregulation that is hypothesized to be linked to depression
ff
Said that the serotonin 5-HT projections slide was important
ff
important to think not just about the types of transmitters but also the brain circuits they are part of
Need to know
the circuits that the monoamine NTs involved in depression are part of
Where are the cell bodies of the serotonin receptors located?
cell bodies located in the brain stem and project to…
how main serotonin brain circuits are there? describe them
2 parallel systems
Describe the brain circuits hypothesized to be linked with each symptom of depression?
see slides
Describe the brain circuits hypothesized to be linked with each symptom of depression?
see slides
why have people siggested that receptor sensitivity mediates the clinical effect of antidepressants?
Because the amount of neurotransmitter increases right away, but clinical effects take more time, and that timeline is more closely associated with changes in receptor sensitivity (note fewer receptors) + there are also genetic changes that happen within the cell
What are charactertistics of all SSRIs
ddd
What are some of the unique elements of different SSRIs
- They
What are some of the unique elements of different SSRIs
- They
Describe the mechanism of action of SSRIs
serotoniergic neuron -> different receptors
somato dendrytic part of neuron -> also has receptors called ‘autorecpectors’ (on the presynaptic neuron, blocking reuptake increases the presence of serotonin in that area which interacts with the autoreceptors)
- > important because the autoreceptors act as a ‘break’ which detects levels of serotonin and stop the release of serotonin
- > when this happens the autoreceptors become very sensitized very fast (by sensitized mean down regulation of the receptors)
meaning that we’re cutting the break cable, which allows for even more serotonin at the post synaptic neuron
Then over time there will be a downregulation of the post synaptic neuron (which is associated with clinical effect)
which antidepressant has to longest half life?
fluoxetine (prozac)
List the pregnancy risk categories
- Category A: adequate, well controlled studies failed to demonstrate a risk of fetus in first trimester
- Category B:
- Category C:
What are the side effects of Prozac?
- sexual (delayed ejaculation, decreased libido, anorgasmia, ED)
- GI disturbance
- Insomnia, anxiety, agitation
- Sweating
- Seizures, activation of maria, suicidal behaviour
Whar are the drug interactions with Prozac
- avoid other medications that might also increase serotonin in the brain: increased risk of serotonin syndrome
- Avoid MAOIs (because the MAOIs are irreversible…. no way or reducing serotonin in the brain) Need to wait 10-14 days for the enzyme to come back before switching the SSRI
- Use with caution with blood thinners
What is serotonin syndrome?
hyperthermic
over reactive reflexes
confusion, agitation
What is a racemis mixture
drug molecule is present in both its forms (right handed form and a left handed form)
What is a racemic mixture
drug molecule is present in both its forms (right handed form and a left handed form)
What is the difference between celexa and cipralex
celexa is a racemic micture
cipralex only contains the left handed form of the molecule
Effexor
how does the receptors affected differ based on dose?
Effexor
how does the receptors affected differ based on dose?
How do MOIs impact blood pressure?
prevent tyromine from breaking down which can impact blood pressire
