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Neurosci Lett. 1991 Sep 2;130(1):120-4.

Depletion of connexin43-immunoreactivity in astrocytes after kainic acid-induced lesions in rat brain.

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  • 1Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.


Recent studies have established that the gap junction protein connexin43 is a major structural component of gap junctions between astrocytes in rat brain. Here, we investigated by immunohistochemical methods the effect of kainic acid-induced neuronal degeneration on connexin43 expression by astrocytes. Stereotaxic injections of kainic acid into the thalamus were found to cause a near total depletion of connexin43-immunoreactivity at the lesion site. Areas depleted of connexin43 corresponded to those exhibiting substantial neuronal loss and intense gliosis. These results implicate a neuronal contribution to the regulation of connexin43 expression by astrocytes and, hence, to local control of the potassium spatial buffering capacity afforded by astrocyte gap junctions.

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