Carbachol induces a form of long-term potentiation in lateral amygdala.

We examined the effects of carbachol, a muscarinic acetylcholine receptor agonist, on excitatory synaptic transmission at thalamo-amygdala synapses in rat brain slices. The application of a low concentration of carbachol (0.25 microM) produced a form of long-term potentiation (cLTP) and a transient suppression of synaptic responses, which was blocked by a muscarinic receptor antagonist, atropine (10 microM). M2 receptor agonist produced only a transient suppression, whereas M1 receptor agonist induced both a transient suppression and a long-term potentiation. Induction of cLTP required simultaneous low-frequency afferent stimulation, and was also dependent upon the activation of NMDA receptors. SQ22536 (50 microM), an adenylyl cyclase inhibitor completely blocked cLTP. Consistently, pretreatment with a maximal concentration of forskolin (10 microM) reduced cLTP.