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Ach has mainly excitatory effects, which are mediated by various subtypes of either nicotinic (N-R, ligand-gated channels) or muscarinic (M-R, G-protein-coupled) receptors. Some M-Rs are inhibitory.
The M-R in the brain are predominantly of M1 type. They act presynaptically to inhibit Ach release from cholinergic neurons, and M-antagonist, by blocking this inhibition, markedly increase Ach release. Many of behavioral effects associated with cholinergic pathways seem to be produced by Ach acting on M-Rs.
N-Rs are also widespread in the brain, but much sparser than M-Rs, there are many subtypes of these Rs. Mostly, these Rs appear to be located presynaptically and to facilitate the release of other transmitters, such as glutamate and DA.
M-R appear to mediate the main behavioral affects associated with Ach, namely effects on arousal, learning and short memory.