Cortical grafts prevent atrophy of cholinergic basal nucleus neurons induced by excitotoxic cortical damage.
Damage to the neocortex, here induced by the excitotoxin kainic acid in the rat, is known to induce cell shrinkage, without actual loss of cells, in the part of the cholinergic basal nucleus projecting to the damaged area. Fetal cortical tissue, implanted into the neuron-depleted cortex in the form of a dissociated cell suspension, completely prevented this degenerative change of the basal nucleus cholinergic neurons. Choline acetyltransferase biochemistry and acetylcholinesterase fiber staining of the transplants indicated a substantial ingrowth from the cholinergic host neurones into the graft. It is proposed that the basal forebrain cholinergic neurons normally receive a trophic influence from their target areas and that grafted neocortex can substitute for the loss of such trophic influence in cortex-damaged animals.
D000544:Alzheimer Disease / Q000139:chemically induced / Q000473:pathology / Q000628:therapy*; D000818:Animals; D002540:Cerebral Cortex / Q000473:pathology / Q000637:transplantation*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004195:Disease Models, Animal; D005333:Fetus; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology; D051381:Rats; D013377:Substantia Innominata / Q000473:pathology
D002795:Choline O-Acetyltransferase; D005968:Glutamate Decarboxylase; D007608:Kainic Acid