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.