Ionotropic receptors form a pore

unbound, closed bound, open

Metabotropic receptors are activated

unboundunactivated

boundactivated

AMPA receptor activation alone

Mg++ block intactrapid, brief, and small EPSP (Na +)

NMDA receptor activation alone

Mg++ block intactno electrical effect

Mg++ block relievedlarge EPSP (Na +, Ca ++); Ca++ release from internal stores

Coincident AMPA & NMDA receptor activation

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 Contracts ciliary muscle, which allows more aqueous humour drainage, thereby decreasing intraocular pressure

Apraclonidine, brimonidine

α2 agonist Inhibits secretion of aqueous humour from the ciliary body and facilitates drainage of same, thereby decreasing pressure in the eye

Betaxolol 1 antagonist

Inhibits secretion of aqueous humour from the ciliary body

Timolol, levobunolol

1-2

antagonistInhibits 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.