Fundamental differences in spontaneous synaptic inhibition between deep and superficial layers of the rat entorhinal cortex

We have previously shown that there are clear differences between spontaneous excitatory synaptic currents recorded in layers V and II of the rat entorhinal cortex (EC) in vitro, and have suggested that these might contribute to a more pronounced susceptibility of the deeper layer to epileptogenesis. In the present study, we have made a detailed comparison of spontaneous synaptic inhibition between the two layers by recording spontaneous inhibitory synaptic currents (sIPSCs) using whole‐cell patch‐clamp techniques in EC slices. Pharmacological studies indicated that sIPSCs were mediated exclusively by γ‐aminobutyric acid (GABA)A receptors. There was little difference in average amplitudes, rise or decay times of sIPSCs in layer II compared with layer V. However, in the former, events occurred at 4–5 times the frequency seen in the latter, and frequencies of ≤40 Hz were not uncommon. When activity‐independent, miniature IPSCs were isolated in tetrodotoxin (TTX), the frequency in layer V was more than halved, but in layer II only a small reduction was seen, and the frequency remained very high. In terms of kinetics, while averaged sIPSCs in each layer were very similar, detailed comparison of individual sIPSCs within layers revealed distinct differences, possibly reflecting inputs from different subtypes of interneurons or inputs at different somatodendritic locations. In layer V, sIPSCs could be divided into three groups, one with slow rise and decay kinetics and a second with fast rise kinetics, further distinguished into two groups by either fast or slow decay kinetics. The distinction between events in layer II was simpler, one group having both fast rise and decay times and the second with both parameters much slower. Finally, IPSCs could occur in high‐frequency bursts in both layers, although these were much more prevalent in layer II. The results are discussed in terms of the overall level of background inhibition in the two layers, as well as how this might relate to their susceptibilities to epileptogenesis. © 2004 Wiley‐Liss, Inc.