A quantitative study of morphological reorganization following chronic optic deafferentation in the adult cat dorsal lateral geniculate nucleus.
Neuronal and synaptic reorganization in the lateral geniculate nucleus (dLGN) of adult cats following chronic visual deafferentation has been investigated with the aid of GABA immunocytochemistry and quantitative electron microscopy. The main purpose of this study was to establish the morphological counterpart of the functional plasticity of dLGN relay cells after total visual deafferentation (Eysel: Brain Res. 166:259-271, '79). The results provide evidence that the regained excitability of relay cells is not the result of disinhibition (caused hypothetically by the selective loss of GABAergic cells) since the proportion of GABA-positive and GABA-negative cells as well as the inhibitory synaptic density did not change. The alternative suggestion that the enhanced excitability could be the result of compensatory axonal sprouting by corticothalamic fibers had also to be dropped: the absolute number of corticothalamic axons to the deafferented dLGN remains unchanged. Because of shrinkage of the dendritic trees of dLGN neurons, however, the density of cortical synaptic input at dLGN cells becomes elevated by almost 60%. It is suggested that the regained excitability of relay neurons is the consequence of the combined effects of adaptive (structural) reduction in size ("atrophy") of retinally denervated nerve cells, and, as a consequence, increase of input resistance, reduced shunting effects, and relative increase in density of the excitatory cortical input per neuron.
D000818:Animals; D002415:Cats; D005829:Geniculate Bodies / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D009473:Neuronal Plasticity; D009900:Optic Nerve / Q000502:physiology*; D020221:Optic Nerve Injuries; D013569:Synapses / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005680:gamma-Aminobutyric Acid