RETINAL GANGLION-CELL DEPLETION ALTERS THE PHENOTYPIC-EXPRESSION OF GABA AND GAD IN THE RAT RETINA

We have looked at the phenotypic expression of gamma-aminobutyric acid (GABA) and the two isoforms of its synthetic enzyme [glutamic acid de carboxylase (GAD)-65 and -67] in adult rat retinas that had the superi or colliculus, pretectum and optic tract lesioned unilaterally at birt h, It has been shown previously that this type of manipulation induces retrograde degeneration of retinal ganglion cells presumably without affecting other intraretinal neurons. We present evidence that GABAerg ic amacrine cells are affected by such manipulation. The number of cel ls immunoreactive for GABA, GAD-65 and GAD-67 decreased in the inner n uclear layer. In the retinal ganglion cell layer, however, the number of GABA- and GAD-65-labelled cells increased, while the number of GAD- 67-labelled cells did not change. Biochemical assay showed that overal l GAD activity was not altered in retinas of lesioned animals. Our res ults support the notion that, while neonatal lesion reorganizes the ex pression of GABA and GAD in the retina, enzyme activity is maintained within normal levels.