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J C Waymire

Publications and source records attributed to J C Waymire.

34 records · Page 2Linked to original sources
PubMed1978

Hippocampal aging and adrenocorticoids: quantitative correlations.

Altered neural-endocrine relations have been proposed as factors in mammalian aging. In the same rats from three age groups we quantified astrocyte reactivity in hippocampus, performed radioimmunoassays for plasma adrenocorticoids, and measured adrenal weight. These variables were correlated in individual animals and generally increased with age. The findings are consistent with recent hypotheses that endocrine levels are related to brain aging, either as cause or effect.

Adrenal Glands↗
PubMed1978

Tryptophan and 5-hydroxyindoles in different CNS regions following acute morphine.

Morphine induces naloxone-reversible increases of tryptophan and 5-hydroxyindoles in rat cerebral hemispheres, thalamus and cerebellum, but does not do so in striatum, hypothalamus, hippocampus and brain stem. Morphine also induces a rise in spinal cord 5-HIAA which is antagonized by naloxone, but there is no parallel change in tryptophan. Increases in brain 5-hydroxyindoles may be related to greater availability of tryptophan, but the elevation in spinal cord 5-HIAA appears to be unrelated to precursor availability.

Animals↗
PubMed1975

Effects of 6-hydroxydopamine and reserpine on amphetamine-induced release of norepinephrine in rat cerebral cortex.

Amphetamine released 3-H-norepinephrine from rat cerebral cortex tissue which had previously accumulated the 3-H-amine. Destruction of noradrenergic nerve endings by pretreatment of the rats with 6-hydroxydopamine inhibited the accumulation of 3-H-norepinephrine by the tissue and reduced the proportion of the 3-H-amine which was released by amphetamine. Inhibition of storage of 3-H-norepinephrine within nerve endings by pretreatment of the animals with reserpine also reduced accumulation of 3-H-norepinephrine but did not reduce the proportion of the accumulated 3-H-amine which was released by amphetamine. The addition of desipramine (an inhibitor of neuronal uptake) further reduced the accumulation of 3-H-norepinephrine in animals pretreated with reserpine but had no further effect in animals pretreated with 6-hydroxydopamine. A greater proportion of the 3-H-norepinephrine was converted to 3-H-deaminated metabolites in tissues of reserpine-treated animals than in the tissues of control or 6-hydroxydopamine-treated rats. Amphetamine-induced release of 3-H-norepinephrine was partially calcium dependent in tissues from control animals. After reserpine treatment, amphetamine-induced release of norepinephrine was independent of calcium, whereas potassium-mediated release was still markedly calcium dependent. These experiments indicate that amphetamine releases 3-H-norepinephrine primarily from storage sites within central adrenergic nerve endings. An analysis of the time course of release from tissues of rats treated with reserpine suggests that amphetamine is equally capable of releasing 3-H-norepinephrine from granular sites which are susceptible to reserpine and from reserpine-insensitive sites.

Amphetamine↗
PubMed1972

Regulation of tyrosine hydroxylase activity in cultured mouse neuroblastoma cells: elevation induced by analogs of adenosine 3':5'-cyclic monophosphate.

Mouse neuroblastoma cells in culture have been used as a model for the study of the mechanism by which activities of tyrosine hydroxylase (EC 1.14.3.a) are regulated in sympathetic tissue. The activity of tyrosine hydroxylase in cultured cells drops to barely detectable activities after 1 week and remains low for months in culture in the uncloned cell line of neuroblastoma. Activity in an adrenergic clone isolated from the uncloned line has about 20% of the activity of the fresh grated tumor cell. N(6), O(2')-dibutyryl adenosine 3':5'-cyclic monophosphate causes a concentration and time-dependent increase in enzyme activity in both the cloned and uncloned cell lines. Enzyme activity is elevated by other stable analogs of adenosine 3':5'-cyclic monophosphate, notably the N(6)-monobutyryl, 8-aminomethyl, and 8-methylthio derivatives of the cyclic nucleotide; by the inhibitor of cyclic nucleotide phosphodiesterase, papaverine; and by sodium butyrate. Changes in cell morphology and tyrosine hydroxylase activity are shown not to be necessarily related.

Animals↗
PubMed1972

Tyrosine hydroxylase in human adrenal and pheochromocytoma: localization, kinetics, and catecholamine inhibition.

The properties of partially purified tyrosine hydroxylase from six pheochromocytomas were compared with partially purified normal human and bovine adrenal medulla enzyme. Substrate and inhibition kinetics, cofactor requirements, and intracellular localization of the enzyme from normal and tumor chromaffin tissue of humans were similar, as was the amount of enzyme activity per gram of tissue. Contrary to previous reports, the sensitivity to catecholamine inhibition of the pheochromocytoma enzyme from the six tumors studied was similar to that of both human and bovine adrenal medulla tyrosine hydroxylase. These results suggest that the excessive synthesis and secretion of catecholamines in some pheochromocytomas is not the result of a reduced sensitivity of tyrosine hydroxylase to catecholamine inhibition.

Adrenal Medulla↗
PubMedDate not supplied

Morphine induced increases in the incorporation of 3H-thymidine into brain striatal DNA.

3H-thymidine uptake into DNA fractions of rat brain regions was measured following in vivo administration of (methyl-3H)-thymidine and morphine. Acute morphine administration (10 mg/kg; 30 min prior to 3H-thymidine) increased incorporation of 3H-thymidine into DNA of rat striatum. This effect was antagonized by naloxone (1 mg/kg). Further, the observed change in incorporation of 3H-thymidine into DNA in striatum could not be accounted for by differences in the local availability of the label in morphinized rats. An autoradiographic study revealed that the 3H-thymidine was localized in nuclei in cells of the sub-ependymal layer lining the lateral ventricles, an area of glial cell proliferation in adult rats. No change in 3H-thymidine incorporation into DNA was observed in any area of the brain in morphine-addicted rats or in rats undergoing naloxone-precipitated withdrawal. The results indicate that opiates may induce permanent anatomical changes in the brain, including alterations of neuroglial interactions.

Animals↗