Fimbria-fornix lesions in aged rats cause increased carbachol-stimulated phosphoinositide hydrolysis in the hippocampus, but no change in muscarinic receptor binding.
Electrolytic lesions of the fimbria/fornix in 26-month-old rats led to an enhanced phosphoinositide (PI) hydrolysis in response to carbachol in hippocampal slices, 11-15 days after surgery. The lesions caused a 78% reduction of choline acetyltransferase but no change in muscarinic binding. The PI response to carbachol and the enhancement of this after lesioning were not as great as that previously reported in young adult rats.
Court
J A
JA
MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne, U.K.
Keith
A B
AB
Kerwin
J M
JM
Perry
E K
EK
D000375:Aging / Q000378:metabolism*; D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D006868:Hydrolysis; D008297:Male; D010716:Phosphatidylinositols / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011976:Receptors, Muscarinic / Q000378:metabolism*
D010716:Phosphatidylinositols; D011976:Receptors, Muscarinic; D002217:Carbachol; D002795:Choline O-Acetyltransferase