[125I]-omega conotoxin binding to human frontal cortex from normal, Alzheimer's and non-Alzheimer's dementia patients.
We studied the binding of the calcium antagonist neurotoxin [125I]-omega conotoxin (GVIA) in age-matched human brains from normal, Alzheimer's disease and non-Alzheimer's dementia patients. Crude preparations of plasmalemmal membranes from frontal cortex were utilized. Saturation isotherms were subjected to Scatchard analysis to determine maximal binding capacity (Bmax) and binding affinity (Kd). In all brain samples tested, [125I]-GVIA binding was homogenous to a single class of high affinity binding sites. Scatchard analysis of saturation isotherms gave the following estimates for normal brains (mean +/- S.D., n = 7): Bmax = .630 +/- .200 pmol/mg and Kd = .177 +/- .054 nM. No significant change was observed in the Kd or Bmax estimates for [125I]-omega conotoxin binding in Alzheimer's disease or non-Alzheimer's dementia brains when compared to normal brains. Although these findings do not rule out the existence of localized changes in calcium channel receptor binding in the frontal cortex of Alzheimer's disease patients, the results do suggest that the neuronal voltage sensitive calcium channel may be unaltered in Alzheimer's disease.
Colvin
R A
RA
Department of Pharmacology, Oral Roberts University School of Medicine, Tulsa, OK.
Allen
R A
RA
Williams
R G
RG
Eagle
D T
DT
Oibo
J A
JA
Miner
G D
GD
D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism*; D001665:Binding Sites; D015220:Calcium Channels / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D003704:Dementia / Q000378:metabolism*; D006801:Humans; D010456:Peptides, Cyclic / Q000378:metabolism*; D020866:omega-Conotoxin GVIA
D015220:Calcium Channels; D010456:Peptides, Cyclic; D020866:omega-Conotoxin GVIA