REACTIVE CHANGE OF THE SUBSTANTIA-NIGRA NEURONS SUBSEQUENT TO STRIATAL INFARCTION IN RATS

The substantia nigra pars reticulata (SNr) receives the inhibitory gam ma-aminobutyric acid (GABA)ergic input from the striatum and globus pa llidus, deafferentation of which is supposed to lead to anterograde tr ansneuronal degeneration of the neurons in the nucleus. In the present study, we studied the pathological changes in the deafferented neuron s in the rat SNr following massive striatopallidal ischemic lesion pro duced by transient middle cerebral artery (MCA) occlusion. At 3 days p ost-ischemia, in association with a decrease of GABAergic afferent fib ers, over one-fourth of the neuronal population in the ipsilateral SNr consisted of swollen chromatolytic cells, while no apparent changes w ere found at day 2. Electron microscopy revealed characteristic ultras tructural findings, including the breakdown of the Golgi apparatus, an accumulation of swollen mitochondria, and disruption of the polysomal clusters of ribosomes. The pathology of these chromatolytic neurons c learly coincides with that of so-called 'reactive change (RC)'. Shrunk en dark neurons were widely distributed at 7 days after surgery, and a significant reduction in the number of neurons was found in the SNr a t 15 days (P < 0.01). The present study suggested that chromatolytic f eature of the SNr neurons may be a consequence of cellular hyper-excit ation after the removal of GABAergic inputs, which may lead these neur ons finally to cell death.