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Biomedical subjects

D H Ross

Publications and source records attributed to D H Ross.

At least 55 records · Page 3Linked to original sources
PubMed1977

Adaptative changes in Ca++-membrane interactions following chronic ethanol exposure.

The data reported here together with recent reports from other investigations suggest that ethanol may act selectively to alter Ca++ metabolism in nerve cells. Changes in calcium content and binding after acute and chronic exposure to ethanol suggest that nerve cells may adapt to ethanol exposure through increasing endogenous calcium content on the synaptic membranes. Since calcium plays an integral role in neurotransmitter metabolism, it may be suggested that adaptation to ethanol may occur via such Ca++ dependent processes as altered membrane transport capabilities and excitation-secretion coupling mechanisms. Future research in these areas would hopefully be directed toward the role of Ca++ in neurotransmitter release and subsequent activation of cyclic nucleotide metabolism.

Alcoholism↗
PubMed1976

Calcium depletion of synaptosomes after morphine treatment.

It was confirmed that morphine administration in vivo produced a selective decrease in the calcium content of synaptosomal fractions prepared from rat cerebral cortices. This effect was prevented by naloxone. 2 After morphine or naloxone, there were no changes in the sodium, potassium and magnesium contents of any of the seven subcellular fractions tested. 3 Since the selective calcium loss was found to occur from fractions similar to those reported to exhibit opiate receptor binding, it is concluded that calcium may play a role in the action of narcotic agonist drugs.

Animals↗
PubMed1976

Effects of chronic morphinization on calcium membrane interaction.

Tolerance to morphine proceeds with an adaptation in the nerve membrane causing an increase in endogenously bound calcium. Our data on calcium binding is compatible with Collier's hypothesis (10) for drug induced changes in number and/or types of receptors. The results demonstrating naloxone reversal of this membrane adaptation suggest that opiate antagonist action may be to maintain the opiate macromolecule portion of the membrane in a Ca++ associated homeostatic state. Lack of effects of Na+ on opiate treated SPM suggest that cellular adaptation to morphine proceeds in vivo through a change in membrane binding of calcium.

Animals↗
PubMed1975

Tolerance to morphine-induced calcium depletion in regional brain areas: characterization with reserpine and protein synthesis inhibitors.

1 Administration of a single dose of morphine sulphate (25 mg/kg) induces tolerance to calcium depletion lasting seven days. 2 There are no apparent changes in calcium content in any of eight discrete brain regions throughout this seven day period. 3 Pretreatment with reserpine (5 mg/kg) did not alter the ability of morphine to induce tolerance. Reserpine alone produced no tolerance to its own calcium depleting action. 4 Cycloheximide (500 mug/kg) but not chloramphenicol (200 mg/kg) effectively prevented development of tolerance. 5 It is concluded that the induction of tolerance to calcium depletion seen after morphine may involve changes in various proteins in membranes of synaptic origin.

Animals↗
PubMed1974

Morphine and ethanol: selective depletion of regional brain calcium.

Administration of morphine or ethanol to rats produces a decrease in regional brain calcium in vivo. This effect is selectively antagonized by the stereospecific narcotic antagonist naloxone. Reserpine and the dopamine-acetaldehyde conjugate salsolinol also produce a depletion of regional brain calcium, but only the salsolinol depletion is antagonized by naloxone. Experiments with naloxone provide evidence for two calcium-sensitive pools in the central nervous system.

Acetaldehyde↗
PubMedDate not supplied

Modification of glycoprotein residues as Ca2+ receptor sites after chronic ethanol exposure.

Previous studies have demonstrated that chronic low-dose administration of ethanol in the drinking fluid of rats produces an increase in content of calcium on synaptic membranes. In the present study, ethanol was studied in vitro and in vivo for its effects on Ca2+ binding to a high affinity receptor site on synaptic membranes. Ethanol (1-50 micrometer) significantly inhibits the binding of Ca2+ in non-competitive fashion, together with inhibiton of a cooperative mechanism for Ca2+ binding. Ruthenium red and neuraminidase were used to probe surface glycoprotein sites as receptors for Ca2+. Use of these probes together with ethanol in vitro or in vivo suggests that increases in Ca2+ receptor sites after chronic ethanol exposure are related to an increase in sialic acid exposure, possibly as a result of conformational changes in membrane protein. These findings are consistent with the hypothesis that chronic low-dose exposure to ethanol causes changes in proteins of synaptic membranes, which may in turn regulate the cellular adaptation to ethanol.

Alcohol Drinking↗
PubMedDate not supplied

Ethanol-induced hypothermia in rats: possible involvement of opiate kappa receptors.

The effect of the opiate antagonists naloxone and MR2266 on ethanol-induced hypothermia and changes in Ca2+-stimulated Mg2+-ATPase activity in brain regions were investigated in the present study. Administration of different doses of ethanol (0.5-2 g/kg, IP) produced a dose-dependent hypothermia. Ca2+/Mg2+-ATPase activity in the hypothalamus was stimulated at 30 min and 2 hr after ethanol (2 g/kg, IP) treatment. In cortex, enzyme activity was inhibited by ethanol at 30 min with no change seen at 2 hr. Naloxone (7.5 mg/kg, SC) at a dose which did not affect body temperature or enzyme activity, partially inhibited ethanol-induced hypothermia and enzyme activity at the earliest time (30 min) but not at 2 hours. The opiate Kappa antagonist MR2266 (5 mg/kg, SC), however, significantly protected against ethanol hypothermia and enzyme activation measured at 30-120 min. This evidence suggests that ethanol-induced hypothermia and subsequent activation changes of Ca2+/Mg2+-ATPase in the hypothalamus may be regulated by opiate Kappa receptors, and that Ca2+ ions play an important role in mediating the effects of ethanol.

Animals↗
PubMedDate not supplied

Effects of alcohol on alpha-adrenergic receptor regulation of calcium ATPase in liver plasma membranes.

The effects of alpha 1- and alpha 2-adrenergic agonists, viz., phenylephrine and clonidine, respectively, were studied on rat liver plasma membrane Ca++-ATPase. Phenylephrine produced a 23% inhibition of enzyme activity at 5 microM. Prazosin, an alpha 1 antagonist, completely prevented the effect of phenylephrine. Clonidine produced a comparable inhibition of Ca++-ATPase, but was not reversed by the antagonist yohimbine, suggesting a lack of functionally significant alpha 2 receptors as previously reported. The results support the role of high-affinity Ca++-ATPase in liver plasma membranes in the control of cytosolic free Ca++ levels through regulation by alpha 1-adrenergic receptors. In vitro and acute ethanol exposure produced inhibition of plasma membrane Ca++-ATPase. In addition, ethanol treatment significantly reversed the inhibitory effect of phenylephrine on Ca++-ATPase. Chronic ethanol exposure for four weeks increased Ca++-ATPase activity over control and increased enzyme activity in the presence of phenylephrine. These results demonstrate that ethanol alters the alpha-adrenergic receptor interaction with Ca++-ATPase resulting in reduced receptor regulation of cytosolic Ca++ levels. These changes may prevent the liver from maintaining Ca++ levels for second messenger functions, such as glycolysis and gluconeogenesis.

Animals↗