Abstract Conventional intracellular recordings were made from neurons of the rat subiculum in an in vitro slice preparation. Intracellular pulses of depolarizing current (duration, 10–120 ms) delivered at a resting membrane potential of −62.2 ± 7.7 mV (mean ± SD, n = 14) imduced bursts of 3–5 fast, action potentials riding on a slow depolarization. The burst was terminated by an afterhyperpolarization (burst AHP) that lasted 117 ± 26 ms and reached peak amplitude of 5.1 ± 1.8 mV ( n = 8). Bath application of the cholinergic agonist carbachol (CCh; 30–100 μM; n = 20) in the presence of ionotropic excitatory amino acid receptor antagonists induced a steady depolarization (4.6 ± 2.7 mV) of the membrane potential, and a small increase in input resistance. Action potential bursts continued to occur in response to intracellular depolarizing pulses during CCh application. However, this cholinergic agonist reduced and eventually blocked the burst AHP, which was replaced by action potentials firing. In the presence of CCh (> 70 μM; n = 9) the burst response, was followed by a depolarizing plateau potential (PP) that outlasted the intracellular depolarizing pulse by 731 ± 386 ms (range 160–1900 ms), and could trigger repetitive action potential firing at 35–116 Hz. The effects induced by CCh were reversed by bath application of the muscarinic antagonist atropine (0.5–1 μM; n = 4). Our findings demonstrate that CCh exerts in the rat subiculum an excitatory action that is dependent upon muscarinic receptor stimulation. This cholinergic mechanism may play a physiological role in the subicular processing of signals arising from the hippocampus proper, and may also contribute to the generation of sustained epileptiform discharges induced in the limbic system by cholinergic agents.