Long-term changes in phosphoinositide hydrolysis following colchicine lesions of the nucleus basalis magnocellularis.
The effect of bilateral colchicine lesions of the nucleus basalis magnocellularis (NBM) on agonist-stimulated phosphoinositide (PI) hydrolysis was examined in cortical slices 1, 3, or 14 months after surgery. Colchicine lesions resulted in a loss of acetylcholinesterase staining in the cortex which recovered to control levels by 14 months. Choline acetyltransferase activity in the cortex was decreased by 43% one month after lesioning, but returned to control levels by 3 months. In vitro stimulation with carbachol produced a concentration-dependent increase in PI hydrolysis, which was enhanced 3 and 14 months after NBM lesions. Norepinephrine and quisqualate-stimulated PI hydrolysis was also enhanced 14 months after NBM lesions. These results suggest a slow up-regulation of postsynaptic receptor function following presynaptic loss of transmitter.
Mundy
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WR
Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.
Tandon
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P
Barone
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Tilson
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HA
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D001479:Basal Ganglia / Q000187:drug effects / Q000502:physiology*; D002217:Carbachol / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003078:Colchicine / Q000494:pharmacology*; D006868:Hydrolysis; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D010716:Phosphatidylinositols / Q000378:metabolism*; D016318:Quisqualic Acid / Q000494:pharmacology*; D051381:Rats; D011916:Rats, Inbred F344; D013997:Time Factors
D010716:Phosphatidylinositols; D016318:Quisqualic Acid; D002217:Carbachol; D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase; D003078:Colchicine; D009638:Norepinephrine