Increased expression of growth-associated protein GAP-43/B-50 following cerebral hemitransection or striatal ischemic injury in the substantia nigra of adult rats.

The substantia nigra receives massive inhibitory gamma-aminobutyric acid (GABA)-ergic inputs, deafferentation of which is supposed to lead to anterograde transsynaptic regression of the nigral neurons. An immunohistochemical technique was used to examine growth-associated protein GAP-43 expression following cerebral hemitransection or transient middle cerebral artery occlusion (MCAO) in the substantia nigra of adult rats. GAP-43 expression was transiently elevated in the substantia nigra pars reticulata (SNr) neurons, but not in the pars compacta neurons at 3 and 4 days post-hemitransection. Massive striatal ischemic injury produced by transient MCAO also caused an increase in GAP-43 synthesis in the SNr neurons at 3 and 4 days after operation. The present findings raise the possibility that deafferentation of the GABAergic inputs leading to transneuronal regression of the SNr neurons is responsible for the elevated expression of GAP-43 in the substantia nigra of adult rats.