A synaptically evoked late hyperpolarization in the rat dorsolateral geniculate neurons in vitro.

Intracellular potentials were recorded from presumed relay neurons in the rat dorsolateral geniculate nucleus maintained in vitro preparations. In this material, the neuronal circuit includes the excitatory optic tract which innervates monosynaptically both relay and intrinsic neurons, the latter providing a feed-forward GABAergic inhibition on the former. Electrical stimulation of the optic tract evokes in the dorsolateral geniculate neurons an early excitatory postsynaptic potential followed by an inhibitory postsynaptic potential which precedes a so far unreported long-lasting late hyperpolarization. The properties of the inhibitory postsynaptic potential are consistent with the notion that they are of disynaptic (feed-forward) origin and that they are the consequence of GABAA receptor activation. In contrast, the late hyperpolarization, which was found in almost every neuron, was enhanced by GABAA blockers, without accompanying changes in the resting membrane potential or the input resistance of the recorded cells. The late hyperpolarization had a lower threshold than the excitatory postsynaptic potential, a long latency (m = 38 +/- 4 ms, n = 10) and was of long duration (m = 308 +/- 57 ms, n = 10). The occurrence and threshold for producing these two potentials were uncorrelated, and paired stimulations of the optic tract showed a marked difference of their recovery time-courses. The late hyperpolarization could be elicited only by afferent stimulations; it never followed intracellularly induced depolarizations and/or anodal break calcium spikes. It was associated with a small conductance increase, sufficient, however, to inhibit high-frequency discharges induced by intracellular injection of depolarizing currents. The late hyperpolarization decreased in amplitude with membrane hyperpolarization and ultimately reversed polarity. The apparent reversal potential followed shifts in extracellular potassium concentration in an almost Nernstian relation (47 mV for a tenfold increase in [K]0). Involvement of GABAB receptors in the generation of this potential may be postulated since baclofen readily hyperpolarized the neurons and decreased their input resistance in the presence of GABAA blockers. We conclude that the late hyperpolarization is a postsynaptic potential mediated by an increased conductance to K ions. Our results further suggest that a minimal disynaptic feed-forward circuit impinging on the relay neurons of the dorsolateral geniculate nucleus is sufficient to subserve this late hyperpolarization.(ABSTRACT TRUNCATED AT 400 WORDS)