Term
| how is acteylcholine synthesized? |
|
Definition
| acetyltransferase (ChAT) synthesizes ACh out of acetylCoA and choline |
|
|
Term
|
Definition
| choline esterases terminate transmission |
|
|
Term
| what are the agonists of nicotinic receptors? |
|
Definition
|
|
Term
| what are agonists of muscarinic receptors? |
|
Definition
| ACh, muscarine, pilocarpine, oxotremorine |
|
|
Term
| what are antagonists of nicotinic receptors |
|
Definition
| curare, succinyl choline, rabies virus |
|
|
Term
| what are antagonists of muscarinic receptors? |
|
Definition
|
|
Term
| what agents releases vesicles and depletes amoutn of ACh for future use? |
|
Definition
| Beta-byngarotoxin and black widow spider venom |
|
|
Term
| what does black widow spider venom do? |
|
Definition
| releases vesicles depleting amount of ACh for future use |
|
|
Term
| what does the botulin toxin do? |
|
Definition
| allows fewer vesicels of ACh to be released |
|
|
Term
| what agent allows fewer vesicles to be released? |
|
Definition
|
|
Term
| what drugs reversibly bind to ACh to prolong ACh transmission; i.e. overstimulates ACh transmission? |
|
Definition
|
|
Term
|
Definition
| irreversibly binds to ACh vesicles to prolong transmission |
|
|
Term
| what do the effectors of nicotinic receptors tend to be? |
|
Definition
| conductance pores b/c nicotinic receptors tend to be part of larger proteins which form channels in membranes |
|
|
Term
| muscarinic receptor effectors often have __________ as a coupling mechanism to decrease cAMP in cells and increase cGMP, DAG, IP3, and Ca+2, and alter ion channels |
|
Definition
|
|
Term
| how do you decrease cAMP in target cells? |
|
Definition
| inhibit adenylate cyclase |
|
|
Term
| how do you increase cGMP in target cells? |
|
Definition
| stimulate gaunylate cyclase |
|
|
Term
| how do you increase DAG, IP3, and Ca in target cells? |
|
Definition
| stimulate phospholipase C |
|
|
Term
| what is the most common excitatory NT in CNS? |
|
Definition
|
|
Term
| what is the most common inhibitory NT in CNS? |
|
Definition
|
|
Term
| what is the most common inhibitory NT in PNS? |
|
Definition
|
|
Term
| what are 3 of the main catecholimines? |
|
Definition
|
|
Term
| what do catecholemines have in common as a precursor? |
|
Definition
|
|
Term
|
Definition
| in the CNS and PNS in vesicles of cells which release NE and EPI |
|
|
Term
|
Definition
| CNS and postganglionic and sympathetic cytosolic cells which release EPI stimulated by corticosteroids |
|
|
Term
|
Definition
| adrenal medulla and brain stem |
|
|
Term
|
Definition
| displace NT from vesicles causing initial release but long term depletion |
|
|
Term
| what agent causes NT to be released and depleted in the future? |
|
Definition
|
|
Term
|
Definition
| this "stress" hormone causes increased EPI synthesis in adrenal medulla |
|
|
Term
| what enhances EPI synthesis? |
|
Definition
|
|
Term
|
Definition
| increases NE in cleft but causes a long term depletion |
|
|
Term
| where are cell bodies of NE neurons found? |
|
Definition
|
|
Term
| where are cell bodies of EPI found? |
|
Definition
|
|
Term
| what are the adregernic receptors? |
|
Definition
alpha 1-everything
alpha 2-presynaptic inhibition
Beta 1-heart
beta 2-lungs
beta 3-adipocytes |
|
|
Term
| what are agonists of beta receptors? |
|
Definition
isoproterenol for all Beta receptors
dopabutamine for beta 1
albuterol for beta 2 |
|
|
Term
| what are antagonists for beta receptors? |
|
Definition
propranol for all beta receptors
atenolol for beta 1 |
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