Receptor alterations in subcortical structures after bilateral middle cerebral artery infarction of the cerebral cortex.

Ischemic damage to the prefrontal, motor, and somatosensory cortex induces alterations in the receptor systems of the caudate putamen and some subcortical brain regions. These alterations may represent an attempt of various neuronal systems to compensate for the reduction in innervation caused by the cortical infarction. Assessment of the receptor changes induced by cortical infarction define neuropharmacologic correlates of cortical damage, indicate possible neurotransmitters associated with neuroanatomically defined subcortical pathways, and suggest possible pharmacologic interventions to counteract the consequences of stroke. Bilateral cortical infarction, induced by ligation of both middle cerebral arteries and temporary occlusion of both common carotid arteries, was investigated in the rat. The infarction resulted in dramatic alterations in subcortical receptor populations as determined by autoradiography. Sodium-dependent, high-affinity, choline-uptake (SDHACU) sites and D1-dopamine receptors in the caudate putamen were unaffected by the infarction, whereas muscarinic and glutamate receptors were increased and D2 receptors were decreased in this structure. A reduction in SDHACU sites caused by the lesion was found in regions including the medial septum, vertical nucleus of the diagonal band, thalamus, nucleus basalis magnocellularis, and basolateral amygdala. M1 receptors were increased in the basolateral and central amygdaloid nuclei whereas non-M1 receptors were increased in the basolateral and central amygdaloid nuclei, but were diminished in the medial septum, vertical nucleus of the diagonal band, thalamus, and nucleus basalis magnocellularis. No significant alterations in muscarinic binding were observed in the various laminae of the hippocampus and dentate gyrus.