Autonomic & Pharmacology of the NMJ + ANS Flashcards
<p>What are the nicotinic receptors and where are they?</p>
<p>N1 (ganglia)</p>
<p>N2 (NMJ)</p>
<p>What are the muscarinic receptors and where are they?</p>
<p>M1 (neronal)</p>
<p>M2 (cacrdiac and presynaptic)</p>
<p>M3 (smooth muscle and glands)</p>
<p>What are the alpha receptors?</p>
<p>A1</p>
<p>A2</p>
<p>What are the beta receptors?</p>
<p>B1</p>
<p>B2</p>
<p>B3</p>
<p>What receptors are ionotropic?</p>
<p>Nicotinic</p>
<p>What receptors use G proteins?</p>
<p>All of them apart from nicotinic, which is ionotropic</p>
<p>What receptors do most drugs not distinguish between?</p>
<p>Sub classes of:</p>
<p>muscarinic</p>
<p>alpha</p>
<p>beta</p>
<p>What is the typical process of synaptic transmission?</p>
<ol> <li>Synthesis and packaging of neurotransmitter into synsynaptic terminal</li> <li>Na+action potential invades terminal</li> <li>Depolarise and activates voltage gated Ca2+channels</li> <li>Triggers Ca+dependent exocytosis of vesicles of transmitter</li> <li>Transmitter difuses across synaptic cleft and binds to receptor to provide a post synaptic response</li> <li>Presynaptic autoreceptors inhibit further transmitter release</li> <li>Transmiter is inactivated by uptake into glia or neurones</li> <li>Transmitter is metabolised within cells</li></ol>
<p>What are potential sites of action for pharmacology of the NMJ?</p>
<p>Inhibit choline transporter</p>
<p>Block voltage gated Ca2+channels</p>
<p>Block vesicle fusion</p>
<p>Non polarising nicotinic receptor blocker</p>
<p>Depolarising nicotinic receptor blocker</p>
<p>Prolong the action potential</p>
<p>Block acetylcholinesterase</p>
<p>What are some clinical applications of pharmacolgy at the NMJ?</p>
<p>Non polarising or depolarising blockers used for paralysis during surgery, electroconvulsive therapy or controlling spasms in tetanus</p>
<p>Botulinum toxin used for treating muscle spasms or cosmetic procedures</p>
<p>Anti cholinesterase used for treating myasthenic syndrome, reversing action of non depolarising blocker or countering botulinum poison</p>
<p>Where could pharmacology of the ANS be at?</p>
<p>Ganglionic transmission</p>
<p>Post ganglionic sympathetic transmission</p>
<p>Post ganglionic parasympathetic transmission</p>
<p></p>
<p>What are potential sites of action for ganglionic transmission?</p>
<p>Inhibit choline transporter</p>
<p>Block voltage gated Ca2+channels</p>
<p>Block vesicle fusion</p>
<p>Block aceylcholine activated channel</p>
<p>Non depolarising nicotinic receptor blockers</p>
<p>Deploarising nicotinic receptor blocker</p>
<p>Activate nicotinic receptors</p>
<p>What are potential clinical applicaitons of pharmacology of ganglionic transmission?</p>
<p>Almost none because the drugs affect both the sympathetic and parasympathetic, and possible th NMJ so there are so many side effects</p>
<p>What are post ganglionic parasympathetic transmission potential sites of action?</p>
<p>Muscarinic receptor antagonist</p>
<p>Muscarinic receptor agonist</p>
<p>What are clinical applicaitons of post ganglionic parasympathetic pharmacology?</p>
<p>Agonist mimics the effects of the parasympathetic system</p>
<p>Antagonist blocks the effects of the parasympathetic system</p>