Nicotinic receptor-mediated responses in relay cells and interneurons in the rat lateral geniculate nucleus.

We used the in vitro whole-cell recording technique to study the nicotinic responses of relay cells and interneurons in the adult rat dorsal lateral geniculate nucleus, the thalamic nucleus that conveys visual signals from the retina to the cortex. These geniculate relay cells and interneurons were identified by their physiological and morphological properties. We found that, in the presence of a muscarinic antagonist, atropine, acetylcholine induced a depolarization in relay cells. A similar depolarization was induced by application of nicotine. These depolarizations were completely blocked by a nicotinic antagonist, hexamethonium, but were little affected by bath solution that contained tetrodotoxin and/or low calcium concentration to block synaptic transmission. This suggests that the depolarization is mediated directly by nicotinic receptors in relay cells. Application of nicotine also induced a depolarization in geniculate interneurons. The interneurons continued to exhibit a response to nicotine in the presence of synaptic blockade, although the time-course of the response was altered. The nicotinic responses in relay cells and interneurons shared many similar properties. Both exhibited desensitization, although this characteristic was much more pronounced in the interneurons. In both cell types, the nicotinic response activated a relatively linear conductance with a slight inward rectification. The reversal potential for the conductance was about - 33 mV, which is consistent with a permeability to sodium and potassium ions. The reversal potential shifted negatively by 5-6 mV when the bath solution contained low calcium, which further suggests a permeability to calcium ions. Our results indicate that nicotinic receptors are present in both geniculate relay cells and interneurons. The nicotinic depolarization in relay cells may serve to enhance transmission of visual signals through the lateral geniculate nucleus as well as to contribute to a voltage-dependent shift in the response mode of geniculate relay cells from burst to tonic (single-spike) firing. The nicotinic depolarization in interneurons may provide an explanation for reports that activation of the cholinergic system can enhance inhibitory tuning in the lateral geniculate nucleus.