The action of the corticofugal pathway on sensory thalamic nuclei: A hypothesis

Abstract

The N-methyl-D-aspartate receptor has recently attracted great interest due to its nonlinear current-voltage behavior. In order to evoke a large depolarizing postsynaptic current, the synaptic-induced conductance change must be paired with a postsynaptic depolarization. This temporally tuned AND gate could underlie a number of different operations throughout the nervous system. We propose that the synapses made by the optical nerve onto projection cells in the mammalian dorsal lateral geniculate nucleus are of the N-methyl-D-aspartate type. [In this Commentary, we have pooled data regarding sensory thalamic nuclei from a number of different mammalian species. Unless otherwise mentioned, we have referred to the dorsal division of the cat lateral geniculate nucleus.] About half of all synapses in these cells--located almost exclusively in the peripheral two-thirds of the dendritic tree--are associated with axons originating in layer VI of visual cortex. It then follows that the massive corticogeniculate pathway controls the gain of the retinogeniculate pathway via its action on the N-methyl-D-aspartate receptors. Thus, near-simultaneous activation of the retinal and the cortical input will transiently enhance the geniculate cell response. Generalizing to other thalamic sensory nuclei, afferent information will be routed through the thalamus and on to the cortex as long as cortical activity is congruent with sensory input to the thalamus. Experimental evidence argues for such a mechanism to control the gain of the somatosensory input to the ventrobasal thalamic nucleus.