Recruitment of GABAergic inhibition and synchronization of inhibitory interneurons in rat neocortex.

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Abstract
Benardo, Larry S. Recruitment of GABAergic inhibition and synchronization of inhibitory interneurons in rat neocortex. J. Neurophysiol. 77: 3134–3144, 1997. Intracellular recordings were obtained from pyramidal and interneuronal cells in rat neocortical slices to examine the recruitment of GABAergic inhibition and inhibitory interneurons. In the presence of the convulsant agent4-aminopyridine (4-AP), after excitatory amino acid (EAA) ionotropic transmission was blocked, large-amplitude triphasic inhibitory postsynaptic potentials (IPSPs) occurred rhythmically (every 10–40 s) and synchronously in pyramidal neurons. After exposure to the γ-aminobutyric acid-A (GABAA) receptor antagonist picrotoxin, large-amplitude monophasic slow IPSPs persisted in these cells. In the presence of 4-AP and EAA blockers, interneurons showed periodic spike firing. Although some spikes rode on an underlying synaptic depolarization, much of the rhythmic firing consisted of spikes having highly variable amplitudes, arising abruptly from baseline, even during hyperpolarization. The spike firing and depolarizing synaptic potentials were completely suppressed by picrotoxin exposure, although monophasic slow IPSPs persisted in interneurons. This suggests that this subset of interneurons may participate in generating fast GABAA IPSPs, but not slow GABAB IPSPs. Cell morphology was confirmed by intracellular injection of neurobiotin or the fluorescent dye Lucifer yellow CH. Dye injection into interneurons often (>70%) resulted in the labeling of two to six cells (dye coupling). These findings suggest that GABAAergic neurons may be synchronized via recurrent collaterals through the depolarizing action of synaptically activatedGABAA receptors and a mechanism involving electrotonic coupling. Although inhibitory neurons mediating GABAB IPSPs may be entrained by the excitatory GABAA mechanism, they appear to be a separate subset of GABAergic neurons capable of functioning independently with autonomous pacing.