The effect of the centrally active anticholinesterase inhibitor Terahydro-9-aminoacridine (THA) on synaptic transmission was studied in rat amygdala neurons in the in vitro slice preparation. THA reversibly suppressed the excitatory postsynaptic potential (EPSP) in a concentration-dependent manner. Postsynaptic depolarization induced by α-amino-5-methyl-4-isoxazole propionate (AMPA) was not decreased by THA. These results demonstrate that THA has a presynaptic inhibitory action on the physiology of synaptic transmission in the amygdala. Pretreating the slices with atropine did not affect THA's effect, indicating that the presynaptic muscarinic receptors are not involved.
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