[Regional and time-sequential changes in amino acid neurotransmitters after focal cerebral ischemia in the rat]

Focal brain lesion is known to induce changes of blood flow and glucose metabolism in the areas other than the lesioned part itself. A well known example of this remote effect is so called diaschisis. To clarify the role of neurotransmitters in this phenomenon, amino acid neurotransmitters were measured in rat basal ganglia after middle cerebral artery occlusion. In the same ischemia model, blood flow and glucose metabolism have been reported to increase in the ipsilateral substantia nigra and globus pallidus in the postischemia period. Our results showed that GABA and aspartate were reduced in ipsilateral substantia nigra and globus pallidus from the 3rd day on, with glutamate level showing no significant change. In the contralateral substantia nigra, GABA increased significantly from the 1st day through the 28th day, whereas glutamate or aspartate showed no significant change. The same, although less pronounced, tendency was observed in the contralateral globus pallidus. In contralateral striatum, GABA increased only during the 1st week. These results may be interpreted as follows. GABA and aspartate were reduced in ipsilateral substantia nigra and globus pallidus due to the afferent pathway interruption caused by focal ischemia. The reduction of inhibitory GABA probably set neurons in these nuclei in a relatively activated state, resulting in the elevation of glucose metabolism and blood flow. Increment of GABA in contralateral substantia nigra and globus pallidus can be attributed to a compensation for the reduction inn ipsilateral nuclei, because the increment was observed even in a chronic phase. This hitherto unknown phenomenon will raise an interesting problem as to the plasticity of the damaged brain.