ENDOTHELIN RECEPTORS IN KAINIC ACID-INDUCED NEURAL LESIONS OF RAT-BRAIN

Seven days after an intracerebroventricular injection of 0.8 mu g kain ic acid, a time of neural tissue-repair after damage, we applied our r eceptor autoradiographic method to examine changes in the endothelin r eceptors in kainic acid-induced neural lesions of the rat brain. There were bell-shaped areas with the de novo expressed [I-125]endothelin-1 binding sites in the damaged hippocampus CA1, CA3, and CA4 subfields. We also noted a homogeneous zone with a low binding-density, the area sandwiched by the belt-shaped areas. In a ''remote'' area correspondi ng anatomically to the deep soma layer of the piriform cortex plus lat eral parts of amygdaloid complex we noted a well-defined area with ''p unched hole-figure'' of low density [I-125]endothelin-1 binding sites. The lesion was surrounded by areas rich in binding sites. The de novo expressed [I-125]endothelin-1 binding sites were characterized endoth elin, receptor. Microglia were present in the area with ''punched hole -figure'' and in the hippocampus pyramidal cell layer with neuronal de ath. In contrast to microglia, astrocytes were rich with hypertrophia in kainic acid-induced neural lesions anatomically corresponding to ar eas with the de novo endothelin(B) receptor. Taken together with the p resent observations of microscopic evidence of cellular distribution, we suggest that the de novo expressed endothelin(B), receptor was carr ied by astrocytes aggregating in neural lesions. In light of our findi ngs, the possibility that astrocytes can be activated by the endotheli n(B), receptor in response to neural tissue repair after damage to neu rons would have to be considered. (C) 1997 IBRO. Published by Elsevier Science Ltd.