Synchronous potentials and elevations in [K +] o in the adult rat entorhinal cortex maintained in vitro

Abstract

Extracellular field-potential recordings and measurements of the extracellular concentration of potassium ([K +] o) were made in layers II and III of the adult rat entorhinal cortex in a slice preparation. Two types of spontaneous, synchronous potentials were induced by the convulsant drug 4-aminopyridine (4AP, 50 μM). The first type was seen in all slices ( n = 19) and consisted of a negative-going field potential that lasted 0.5–3.5 s and occurred at rates of 0.013–0.13 Hz. This event was accompanied by an elevation in [K +] o that attained peak values of 4.0–7.6 mM. The second type was reminiscent of ictal epileptiform discharges and was recorded in 6 of 19 slices; it lasted 21–190 s, recurred at 0.001–0.003 Hz and was associated with [K +] o increases that had peak values of 14–17 mM. Whenever such an ictal discharge occurred, it was closely preceded and thus appeared to be initiated by the first type of field potential. Perfusion with N-methyl- d-aspartate (NMDA) receptor antagonist (±)-3-(2-carboxy-piperazine-4-yl)propyl-1-phosphonate (CPP; 10 μM) abolished the ictal discharge ( n = 4). This pharmacological procedure did not abolish the negative-going potentials that continued to occur during further application of the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μM; n = 4). These glutamatergic-independent potentials were, however, blocked by the GABA A-receptor antagonist bicuculline methiodide (10 μM, n = 3). Thus, as in the hippocampus, 4AP can induce in the entorhinal cortex a synchronous GABA-mediated potential that is resistant to excitatory amino acid antagonists. In addition, the entorhinal cortex generates ictal discharges that are presumably caused by an NMDA-mediated mechanism. Since these ictal discharges are not observed in the adult rat hippocampus, we conclude that the entorhinal cortex possesses a higher propensity for generating epileptiform activity.