Depletion of connexin43-immunoreactivity in astrocytes after kainic acid-induced lesions in rat brain.
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.
Vukelic
J I
JI
Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Yamamoto
T
T
Hertzberg
E L
EL
Nagy
J I
JI
D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D001927:Brain Diseases / Q000139:chemically induced / Q000378:metabolism*; D017630:Connexins; D007150:Immunohistochemistry; D007608:Kainic Acid / Q000633:toxicity*; D008297:Male; D008565:Membrane Proteins / Q000276:immunology / Q000378:metabolism*; D009410:Nerve Degeneration / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D013788:Thalamus / Q000276:immunology / Q000378:metabolism
D017630:Connexins; D008565:Membrane Proteins; D007608:Kainic Acid