EXCITATORY EFFECTS INDUCED BY CARBACHOL ON BURSTING NEURONS OF THE RAT SUBICULUM

Conventional intracellular recordings were made from neurons of the ra t subiculum in an in vitro slice preparation. Intracellular pulses of depolarizing current (duration, 10 - 120 ms) delivered at a resting me mbrane potential of -62.2 +/- 7.7 mV (mean +/- SD, n = 14) induced bur sts 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 mu M; 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 intracellula r depolarizing pulses during CCh application. However, this cholinergi c agonist reduced and eventually blocked the burst AHP, which was repl aced by action potentials firing. In the presence of CCh (> 70 mu M; n = 9) the burst response, was followed by a depolarizing plateau poten tial (PP) that outlasted the intracellular depolarizing pulse by 731 /- 386 ms (range 160 - 1900 ms), and could trigger repetitive action p otential firing at 35 - 116 Hz. The effects induced by CCh were revers ed by bath application of the muscarinic antagonist atropine (0.5 - 1 mu M; n = 4) Our findings demonstrate that CCh exerts in the rat subic ulum an excitatory action that is dependent upon muscarinic receptor s timulation. This cholinergic mechanism may play a physiological role i n the subicular processing of signals arising from the hippocampus pro per, and may also contribute to the generation of sustained epileptifo rm discharges induced in the limbic system by cholinergic agents.