Reverberation of chloride-dependent synaptic potentials in the rat entorhinal cortex in vitro.

The spontaneous activity generated by rat entorhinal neurons during application of 4-aminopyridine (4AP; 50 microM) was studied with intracellular and extracellular field-potential recordings in an vitro slice preparation. Long-lasting depolarizations (LLDs) with amplitudes of 15 +/- 7.6 mV (mean +/- SD; n = 14) and durations of 1.65 +/- 0.77 s (n = 14) occurred at 0.036 +/- 0.01/s (n = 14). Each LLD was followed by a rhythmic sequence of depolarizing potentials (up to 22 events) with amplitudes of 4-30 mV, durations of 40-500 ms and frequency of 0.9 +/- 0.2/s (n = 14). These intracellular potentials were mirrored by negative-going field potentials, suggesting that they represented synchronous events. Membrane input resistance decreased by 79-86% during both LLDs and subsequent rhythmic depolarizations. Intracellular injection of steady depolarizing or hyperpolarizing current modified the amplitude of these potentials in a similar manner: the reversal potential of the LLDs and of the rhythmic depolarizations was -66.4 +/- 4 mV and -67.9 +/- 3.2 mV, respectively (n = 7). Intracellular injection of Cl- increased the amplitude of both types of potentials. Spontaneous LLDs continued to occur during application of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (10 microM), a procedure that abolished the subsequent rhythmic depolarizations (n = 3). LLDs were blocked by further addition of the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline methiodide (10 microM, n = 3). Our findings demonstrate that during 4AP application entorhinal neurons generate glutamatergic-independent LLDs as well as synchronous, Cl(-)-dependent depolarizations that reverberate through non-NMDA-mediated excitatory circuits.