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C S Cascio

Publications and source records attributed to C S Cascio.

25 records · Page 2Linked to original sources
PubMed1983

Characterization of [3H]tryptamine binding sites in brain.

[3H]Tryptamine binds with high affinity to sites on rat brain membranes. The sites have the characteristics of tryptamine receptor recognition sites. These sites are widely distributed among rat brain regions with the highest density occurring in the cerebral cortex, striatum and hippocampus. The site is also found in human cerebral cortex. The binding site is localized mainly to the synaptosomal fraction. Drug competition studies indicate that the [3H]tryptamine binding site is distinct from serotonin receptors. Drugs that are potent inhibitors of [3H]tryptamine binding include tetrahydro-beta-carboline, quipazine, phenylethylamine, amphetamine, p-chloroamphetamine and methamphetamine.

Animals↗
PubMed1982

Tetrahydro-beta-carbolines: affinities for tryptamine and serotonergic binding sites.

The affinities of four tetrahydro-beta-carbolines at [3H]tryptamine, [3H]5-HT (5-HT1), and [3H]spiperone (5-HT2) binding sites in rat cerebral cortex were investigated. The unsubstituted tetrahydro-beta-carboline was the most potent of the four compounds at all three binding sites, but was 200-400 times more potent at the tryptamine site than at either of the serotonin sites.

Animals↗
PubMed1981

Lithium increases serotonin release and decreases serotonin receptors in the hippocampus.

The effects of long-term lithium administration on pre- and postsynaptic processes involved in serotonergic neurotransmission were measured in rat hippocampus and cerebral cortex. Long-term lithium administration increased both basal and potassium chloride-stimulated release of endogenous serotonin from the hippocampus but not from the cortex. Serotonergic receptor binding was reduced in the hippocampus but not in the cortex. These results suggest a mechanism by which lithium may stabilize serotonin neurotransmission.

Animals↗
PubMed1981

Electroconvulsive shock and reserpine: effects on beta-adrenergic receptors in rat brain.

Electroconvulsive shock (ECS) administered once daily for up to 14 days decreases beta-adrenergic receptor binding in the cortex and hippocampus in a time-dependent manner. The decrease in binding in the cortex lasts at least 1 week after the last shock. In the striatum, hypothalamus, or cerebellum, 14 days of ECS did not produce significant changes in beta-adrenergic receptor binding. The brain regional pattern of beta-adrenergic receptor changes suggests that repeated ECS affects beta 1-adrenergic receptors in brain regions that receive a noradrenergic innervation activated by ECS. The effects of ECS on neurotransmitter receptor binding appear to be highly selective. Of five receptors in the cortex and three receptors in the hippocampus measured, only beta-adrenergic receptor binding is decreased. Chronic footshock stress does not alter beta-adrenergic receptor binding sites in the cortex, indicating that the effects of ECS are not due to stress alone. The effects of ECS on reserpine-induced alterations in beta-adrenergic receptor binding sites were also examined. Ten days of ECS following chronic reserpine injections reverses the increased binding of beta-adrenergic receptors.

Animals↗