Synaptic inputs to single neurons in the lateral geniculate nuclei of normal and monocularly deprived squirrel monkeys.

Neurons in the dorsal lateral geniculate nucleus (dLGN) of normal and monocularly lid-sutured squirrel monkeys were recorded electrophysiologically, and some were injected intracellularly with horseradish peroxidase (HRP) to examine and compare their synaptic inputs. Limited tests of the receptive field properties did not show any differences between the normal, nondeprived, or deprived neurons. Sixteen injected neurons were examined at the light microscopic level with most of these located in the P-laminae (n = 14). Ten of these were either from normal monkeys (n = 9) or received input from the nondeprived eye of a monocularly deprived monkey (n = 1). The remaining six neurons received input from the deprived eye. The dendritic trees of deprived neurons did not differ from those of normal or nondeprived neurons. Three normal and five deprived neurons from the P-laminae were examined at the electron microscopic level. Afferent distributions were not significantly different between normal and deprived neurons. Retinal, cortical, and gamma aminobutyric (GABA)ergic afferents accounted for nearly all inputs (avg., 42%, 23%, and 32%, respectively) and selectively contacted proximal, distal, or all parts of the dendrites. Overall, synaptic densities (synapses per length of dendrite) were high proximally and decreased with distance from the soma. However, the synaptic densities onto deprived neurons were higher at all distances compared to those onto normal neurons. Furthermore, HRP-filled deprived neurons received an average of 25 synapses onto their somata compared with only an average of 7 somal synapses on the HRP-filled normal neurons. Most of the increase in the number of synapses onto the deprived neurons was from GABAergic type profiles. This abnormality of the deprived neurons of the dLGN could be the underlying cause of their lesser responses compared with normal or nondeprived dLGN neurons. It could also be the initial stage that causes blindness in monocularly lid-sutured primates.