DRUGS Flashcards
TTX
Na+ channel inactivation
TEA
K+ channel inactivation, but non selective so it can target Ca2+ channels and also target the nAChRs
Cocaine
Agonist of NA+ channels in use dependent competitive manner - 3% actually binds to Na+ channels O’Leary 2010 - joyous feelings arise from the indirect agonist of dopamine reuptake receptors (DAT)
Derivatives of cocaine used because
Coke takes ages to unbind from Na+ receptors - and hence the effects cannot be appropriately mediated - 8x slower - Crumb and Clarkson 1990
3 major discoveries of the synapse
1936 Loewi and Dale NP - demonstrated that transmission was chemical
Loewi - placed two frog hearts in a bath and slowed the first - the second slowed two and determined the substance was Vagustoff
Dale then determined this was ACh with experiments on leech muscle
Vesicles - then from the coloured with histochemical staining then electron microscopy - Koelle et Al - 1949
Fatt and Katz - 1954 - determined the vesicular and quantal nature of ACh release - mEPPs - determined too big to be of just one ACh molecule and that they were uniform in size
Turbocuraine
NMJ - Non depolarising competitive antagonist of nAChRs - long duration paralytic
Suxamethonium
Depolarising direct cholinergic agonist - intermediate fasiculation
Sarin nerve gas
Inhibits by competitive binding AChE - seizures and resp arrest
Organophosphates
AChE inhibitors also excess muscarinic and nicotinic action
Botulinum toxin
Cleaves SNAP 25 - no partial fusion so no vesicular release
Myaesthenia Gravis
IgG autoantibodies - bind to and increase the rate at which the receptor itself is degraded - treated with AChEs
Atropine
Anticholinergic muscarinic competitive antagonist - acts on M2 (inhibits an inhibitory) - at vagus nerve junction
Pirenzepine
Muscarinic M2 receptor antagonist - inhibits gastric acid secretion
Gallamine
M2 competitive antagonist - muscle relaxation in general anaesthetic
Darifenacin
M3 agonist located in smooth muscle (bladder)