Vl. Dawson et al., RECEPTOR ALTERATIONS IN SUBCORTICAL STRUCTURES AFTER BILATERAL MIDDLECEREBRAL-ARTERY INFARCTION OF THE CEREBRAL-CORTEX, Experimental neurology, 128(1), 1994, pp. 88-96
Ischemic damage to the prefrontal, motor, and somatosensory cortex ind
uces alterations in the receptor systems of the caudate putamen and so
me subcortical brain regions. These alterations may represent an attem
pt of various neuronal systems to compensate for the reduction in inne
rvation caused by the cortical infarction. Assessment of the receptor
changes induced by cortical infarction define neuropharmacologic corre
lates of cortical damage, indicate possible neurotransmitters associat
ed with neuroanatomically defined subcortical pathways, and suggest po
ssible pharmacologic interventions to counteract the consequences of s
troke. Bilateral cortical infarction, induced by ligation of both midd
le cerebral arteries and temporary occlusion of both common carotid ar
teries, was investigated in the rat. The infarction resulted in dramat
ic alterations in subcortical receptor populations as determined by au
toradiography. Sodium dependent, high-affinity, choline uptake (SDHACU
) sites and D-1-dopamine receptors in the caudate putamen were unaffec
ted by the infarction, whereas muscarinic and glutamate receptors were
increased and D-2 receptors were decreased in this structure. A reduc
tion in SDHACU sites caused by the lesion was found in regions includi
ng the medial septum, vertical nucleus of the diagonal band, thalamus,
nucleus basalis magnocellularis, and basolateral amygdala. M(1) recep
tors were increased in the basolateral and central amygdaloid nuclei w
hereas non-M(1) receptors were increased in the basolateral and centra
l amygdaloid nuclei, but were diminished in the medial septum, vertica
l nucleus of the diagonal band, thalamus, and nucleus basalis magnocel
lularis. No significant alterations in muscarinic binding were observe
d in the various laminae of the hippocampus and dentate gyrus. (C) 199
4 Academic Press, Inc.