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Response of retinal terminals to loss of postsynaptic target neurons in the dorsal lateral geniculate nucleus of the adult cat
Author(s) -
Pearson Helen E.,
Stoffler Deborah J.,
Sonstein William J.
Publication year - 1992
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903150308
Subject(s) - biology , geniculate , retinal , retina , giant retinal ganglion cells , neuroscience , axon , anatomy , kainic acid , ganglion , postsynaptic potential , lateral geniculate nucleus , retinal ganglion cell , nucleus , receptor , biochemistry , glutamate receptor
We have used the neurotoxin kainic acid to produce rapid degeneration of neurons in the dorsal lateral geniculate nucleus (dLGN) of the adult cat. This degeneration mimics the rapid loss of geniculate neurons seen after visual cortex ablation in the neonate. Subsequent anterograde transport of horseradish peroxidase injected into the eye was used to reveal the projection patterns of retinal ganglion cell axons at different survival periods after the kainic acid injection. The density of retinal projections to the degenerated regions of the geniculate was reduced considerably at 4 and 6 months survival, but at 2 months was not significantly different from normal. The laminar pattern of projections to degenerated regions of the geniculate did not change in any animals studied, even when an adjacent lamina contained surviving cells. Electron microscopic examination of degenerated dLGN revealed intact retinal (RLP) and RSD terminals at all survival times, although the density of terminals appeared much reduced when compared to controls. Some RLP terminals exhibited the “dark reaction” of degeneration and these degenerating terminals were most numerous at 2 months survival. These findings demonstrate that, in response to degeneration of their usual target cells, mature retinal ganglion cells will withdraw their axon terminals from these regions of degeneration. We conclude that mature retinal ganglion cells continue to be dependent on target integrity for the maintenance of a normal axonal arborization.