Cholinergic ventral forebrain grafts into the neocortex improve passive avoidance memory in a rat model of Alzheimer disease.
The memory dysfunction of Alzheimer disease has been associated with a cortical cholinergic deficiency and loss of cholinergic neurons of the nucleus basalis of Meynert. This cholinergic component of Alzheimer disease can be modeled in the rat by ibotenic acid lesions of the cholinergic nucleus basalis magnocellularis. The memory impairment caused by such unilateral lesions, as reflected in passive avoidance behavior, is reversed by grafts into the deafferented neocortex of embryonic neurons of the cholinergic ventral forebrain, but not by grafts of noncholinergic hippocampal cells.
D000110:Acetylcholinesterase / Q000378:metabolism; D000544:Alzheimer Disease / Q000503:physiopathology*; D000818:Animals; D001362:Avoidance Learning / Q000502:physiology; D002799:Cholinergic Fibers / Q000502:physiology* / Q000637:transplantation; D004195:Disease Models, Animal; D006801:Humans; D007051:Ibotenic Acid / Q000494:pharmacology; D008568:Memory / Q000502:physiology; D051381:Rats; D013377:Substantia Innominata / Q000502:physiology
D007051:Ibotenic Acid; D000110:Acetylcholinesterase