Electrophysiological and pharmacological properties of interneurons in the cat dorsal lateral geniculate nucleus.

We investigated the electrophysiological and pharmacological properties of morphologically identified and putative interneurons within laminae A and A1 of the cat dorsal lateral geniculate nucleus maintained in vitro. These intralaminar interneurons possess unique electrophysiological characteristics, including (1) action potentials of a short duration (average width at half amplitude of 0.34 ms). (2) the ability to generate high-frequency trains of action potentials exceeding 500 Hz, without strong spike frequency adaptation, and (3) a low-threshold regenerative response with variable magnitude of expression, ranging from a subthreshold depolarization towards the generation of one to several action potentials in different cells. The low-threshold regenerative depolarization following a hyperpolarizing current pulse was increased in size by application of 4-aminopyridine, was reduced by nickel, and was not influenced by extracellular cesium. These findings indicate that this event is mediated by an underlying Ca(2+)-dependent mechanism, such as a low-threshold Ca(2+) current, that is regulated by the activation of opposing transient K+ currents. Every interneuron tested responded to glutamate, kainate, quisqualate, or N-methyl-D-aspartate with depolarization and action potential discharge. In contrast, we did not observe a postsynaptic response to activation of the metabotropic receptors with 1S,3R-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate. Application of gamma-amino-butyric acid (GABA) strongly inhibited spike firing through a biphasic hyperpolarization and increase in membrane conductance, a response that reversed close to the presumed chloride equilibrium potential and was imitated by the GABAA receptor agonist muscimol. The GABAB receptor agonist baclofen evoked only a weak membrane hyperpolarization from rest and suppression of spontaneous spike activity. Application of acetylcholine, or the muscarinic agonist acetyl-beta-methylcholine, inhibited spontaneous action potential activity through hyperpolarization of the membrane potential, presumably resulting from an increase in membrane potassium conductance. In contrast, application of serotonin only slightly facilitated tonic activity in a subpopulation of interneurons, histamine induced a small slow depolarization apparently through activation of presynaptic excitatory pathways, and noradrenaline and adenosine had no detectable effect on the spontaneous firing or resting potential of interneurons. We suggest that intralaminar interneurons may function in a relatively linear manner to transform retinal and cortical inputs into a local field of inhibition in the dorsal lateral geniculate and that the excitability of these neurons is largely controlled by retinal, cortical, GABAergic, and cholinergic (brainstem) afferents.