The modulation of the retinal relay to the cortex in the dorsal lateral geniculate nucleus.

The translation of the retinal input through the dorsal lateral geniculate nucleus (dLGN) to the visual cortex is highly dependent on a range of influences. This article reviews the available evidence. One of the influences, the corticofugal projection to the dLGN from layer VI of the visual cortex, provides a synaptic input which in magnitude exceeds that from the retina. This makes direct synaptic contact on relay cells and the intrinsic and perigeniculate inhibitory interneurones influencing their activity. The corticofugal system appears to be spatially organised in such a way that for any given region in the dLGN, there is a central zone comprising an overlying field with facilitatory effect, and a surrounding zone with inhibitory influence. The extent to which these overlap is open to question at present. The inhibitory effect of the corticofugal projection can be clearly seen in its contribution to the length tuning of dLGN cells when tested with drifting bars. On average dLGN cells exhibit a very high degree of length tuning, matching that of cortical hypercomplex cells. Removal of the corticofugal influence causes a radical reduction in this, shifting the mean reduction in peak response with increasing bar length from 71% to 43%. One consequence of this corticofugal effect is that the selectivity of the dLGN cell receptive field towards stimuli spatially restricted to the vicinity of the centre mechanism, is as good for moving bars as it is for stationary flashing spots. The retinal output to dLGN relay cells appears to be mediated by excitatory amino acid receptors, of both NMDA and non-NMDA categories. The non-NMDA receptors appear to provide an initial level of depolarisation which enables the operation of the voltage dependent NMDA receptor channels. The NMDA receptor however sits as a critical gate regulating the transmission of retinal information in the dLGN, when it is blocked visual responses are virtually eliminated. Its voltage dependency makes it crucially dependent on the complex pattern of excitatory and inhibitory influences from the cortex and the "non-specific" modulatory influence of the cholinergic system.