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Ionotropic receptors form a pore unbound, closed bound, open Metabotropic receptors are activated unbound unactivated bound activated AMPA receptor activation alone Mg++ block intact rapid, brief, and small EPSP (Na +) NMDA receptor activation alone Mg++ block intact no electrical effect Coincident AMPA & NMDA receptor activation Mg++ block relieved large EPSP (Na +, Ca ++); Ca++ release from internal stores Neuromuscular junction Stained acetylcholine receptors The GABAA receptor Metabotropic receptor amplification Dark current Light turns off the dark current Glaucoma • Loss of peripheral vision typically associated with elevated ocular pressure due to insufficient drainage • Treatment is aimed at either increasing drainage or decreasing aqueous humour production (even though excess aqueous humour production is rarely the pathological problem) • Note that there is low (or normal) pressure glaucoma, poorly understood. Ciliary body Drugs used to treat glaucoma Drug Receptor Drug action Pilocarpine M3 agonist Apraclonidine, brimonidine α2 agonist Betaxolol b1 antagonist Contracts ciliary muscle, which allows more aqueous humour drainage, thereby decreasing intraocular pressure Inhibits secretion of aqueous humour from the ciliary body and facilitates drainage of same, thereby decreasing pressure in the eye Inhibits secretion of aqueous humour from the ciliary body Timolol, levobunolol b1-b2 antagonist Inhibits secretion of aqueous humour from the ciliary body Note this subset of the drugs used to treat glaucoma are ones that act on the ANS.