Neuropharmacology Flashcards
Synaptic transmission of neurones
Neurotransmitter into pre-synaptic terminal
Na invades
Voltaged gated Ca open
Exocytosis
What happens with neurotransmitter
Binds to inotropic or metatropic (G-protein) on post-synaptic
Pre-synaptic auto receptor prevent further release
Neuotransmitter inactivated by uptake
How do you reduce transmission
Could do this but no drugs Increase breakdown Increase uptake Decrease packaging Increase inhibitory auto receptor
Drugs Block release e.g. boto Block Na - LA Block Ca - spider toxin Block post receptors - antagonist
How do you increase transmission
Increase packaging
Activate post synaptic receptor e.g. agonist
Drugs to increase effect of receptor e.g. barbiturates + benzodiazepine
Block breakdown e.g. Acetylcholinesterase
Block uptake e.g. serotonin
Examples neurotransmitter
Ach NO Amines - NA, dopamine, serotonin AA - glutamate, GABA Purines - ATP / adenosine Neuropeptides - endorphines/ CCK
How does dopamine work
Medulla = vomit SN = movement Limbic = emotion + behaviour
What does Parkinson’s do
Degernation of dopamine neurones in SN
How does dopamine act on brain if unable to cross BBB
Tyrosine crossed
Tyrosine converted to DOPA by TH
Dopa converted to dopamine by AAAD
What do dopamine antagonist do
Improve vomiting
Improve psychosis
Why is domperidone useful as anti-emetic in Parkinson
Doesn’t cross BBB
Improve vomit but doesn’t worsen Parkinson
When are dopamine antagonist used long term
Psychosis
- Often only option but can cause movement disorder
Don’t use long term for sickness as chronic doesn’t exist
What is GABA
Inhibitory
When is it useful
Anti-epilpetic - Sodium valproate
Anti-anxiety
What does serotonin do
Uptake blocker
e.g. triptans for pain
What does NA do
Uptake blocker
Anti-depressant
