Lesion-Induced Relative Supersensitivity to an Excitatory Amino Acid Agonist in the Cat Dorsal Lateral Geniculate Nucleus

Abstract

Chronic monocular deafferentation has been shown to produce an increased excitability in cells of the dorsal lateral geniculate nucleus (dLGN) (Eysel 1979). Furthermore, a recent quantitative morphological study (Somogyi et al. 1987) has shown that chronic monocular deafferentation results in a relative increase in density of the excitatory cortical input to the dLGN neuron. This effect and the changes related to transneural atrophy of the deafferented cells might explain part of the functional changes observed after chronic deafferentation. Nevertheless, denervation supersensitivity might also be involved. Accumulating evidence indicates that the neural transmitter mediating the visual input to dLGN cells acts at an excitatory amino acid receptor (Kemp and Sillito 1982). Natural excitatory amino acids such as L-glutamate and L-aspartate can act at a number of receptors which have been characterized in terms of the specific agonists N-methyl-D-aspartate, quisqualate and kainate (Watkins and Evans 1981). In the present experiments we have addressed the question of possible denervation supersensitivity to excitatory amino acid agonists as a consequence of chronic monocular deafferentation. With the iontophoretic technique the responses of normal and denervated cells in the A-laminae of the dLGN to acetylcholine, N-methyl-D-aspartate and quisqualate were compared. The results indicate that chronic monocular deafferentation increases the relative sensitivity of the denervated cells to quisqualate.