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R A Colvin

Publications and source records attributed to R A Colvin.

40 records · Page 3Linked to original sources
PubMedDate not supplied

[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.

Aged↗
PubMedDate not supplied

Analysis of Na+/Ca2+ exchange activity in human brain: the effect of normal aging.

Na+/Ca2+ exchange activity and passive permeability to Ca2+ were analyzed in plasma membrane vesicles (PMV) purified from whole rat brain and three regions of human brain: frontal cortex, temporal cortex, and cerebellum. Accumulation of Ca2+ due to Na+/Ca2+ exchange activity showed a characteristic pattern of an initial rapid rise in Ca2+ content followed by a stable plateau in both rat and human brain. Total Ca2+ accumulation in rat brain PMV was on average three-fold higher than in human brain. Passive permeability to Ca2+ was measured as the rate of Ca2+ release from PMV first loaded with 45Ca by Na+/Ca2+ exchange and then exposed to 1 mM EGTA. The Ca2+ permeabilities of human and rat brain PMV were similar. Ca2+ release from rat brain PMV was faster overall and was resolved into fast and slow components while in human brain a single slow component was found. Post mortem delay up to 4 h had no effect on Na+/Ca2+ exchange Km for Ca2+, Vmax, and peak uptake and Ca2+ release rate in rat brain PMV. Human frontal cortex was shown to have a greater Na+/Ca2+ exchange activity than that found in the cerebellum. The frontal cortex, temporal cortex and cerebellum had similar Ca2+ permeabilities. Age-related effects on Na+/Ca2+ exchange activity and Ca2+ permeability were determined in 15 tissues from human frontal cortex (age at death 21 to 93 years). No significant age related effects were seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Effects of Ca channel blockers on Ca transport and Ca ATPase in skeletal and cardiac sarcoplasmic reticulum vesicles.

Several Ca channel blockers--verapamil, nifedipine, nimodipine (Bay e 9736), and nitrendipine (Bay e 5009)--had different effects on Ca transport by sarcoplasmic reticulum vesicles from either skeletal or cardiac muscle. Both nimodipine and nitrendipine (1 X 10(-4) M) stimulated Ca sequestration in the absence of a Ca-precipitating anion by either cardiac or skeletal sarcoplasmic reticulum (SR), with nitrendipine being the more potent stimulator. Nifedipine (1 X 10(-4)M) had no significant effect, whereas at higher concentrations (3 X 10(-3) M) verapamil inhibited the Ca sequestration reaction. Nitrendipine stimulated Ca ATPase and Ca sequestration to a similar extent. Stimulation of Ca sequestration by nitrendipine was dependent on drug/membrane phospholipid mole ratios of between 1:4 and 3:1, as well as absolute drug concentration thus suggesting an interaction of the drug with membrane phospholipids. Nifedipine, nitrendipine, nimodipine, and verapamil (1 X 10(-4)M) had no effect on phosphate-supported Ca uptake by skeletal SR, whereas higher concentrations of verapamil (3 X 10(-3)M) inhibited this reaction by either cardiac or skeletal SR. The results of this study suggest that (a) Ca channel blockers have complex and variable effects on SR membranes, (b) these effects are similar in cardiac and skeletal SR, and (c) the effects are in part mediated through an interaction with membrane phospholipids or hydrophobic portions of the Ca ATPase.

Absorption↗