SYNCHRONOUS POTENTIALS AND ELEVATIONS IN [K-RAT ENTORHINAL CORTEX MAINTAINED IN-VITRO(](0) IN THE ADULT)

Extracellular field-potential recordings and measurements of the extra cellular concentration of potassium ([K+](o)) were made in layers II a nd III of the adult rat entorhinal cortex in a slice preparation. Two types of spontaneous, synchronous potentials were induced by the convu lsant drug 4-aminopyridine (4AP, 50 mu M). The first type was seen in all slices (n=19) and consisted of a negative-going field potential th at 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 d ischarges and was recorded in 6 of 19 slices; it lasted 21-190 s, recu rred 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 fir st type of field potential. Perfusion with N-methyl-D-aspartate (NMDA) receptor antagonist -3-(2-carboxy-piperazine-4-yl)propyl-l-phosphonat e (CPP; 10 mu M) abolished the ictal discharge (n=4). This pharmacolog ical procedure did not abolish the negative-going potentials that cont inued to occur during further application of the non-NMDA antagonist 6 -cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 mu M; n=4). These glutam atergic-independent potentials were, however, blocked by the GABA(A)-r eceptor antagonist bicuculline methiodide (10 mu M, 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 an tagonists. In addition, the entorhinal cortex generates ictal discharg es that are presumably caused by an NMDA-mediated mechanism. Since the se ictal discharges are not observed in the adult rat hippocampus, we conclude that the entorhinal cortex possesses a higher propensity for generating epileptiform activity.