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Biomedical subjects

R Morgenstern

Publications and source records attributed to R Morgenstern.

180 records · Page 10Linked to original sources
PubMed1980

Relationship between pD2 and pA2 of neuroleptics.

The differences in the pD2/pA2 ratio of nine tested neuroleptics were found to vary between 0.92 and 1.11. This result confirms the hypothesis that pD2 (as determined from the inhibition of spontaneous locomotor activity) and pA2 (as determined from the shift of apomorphine dose response curve induced by a fixed dose of the neuroleptic) should not differ markedly and is discussed as differences in receptor specifities on the basis of the concept of multiple binding sites fo neuroleptics in the brain.

Animals↗
PubMed1980

Effects of atypical antidepressants on LSD potentiated apomorphine hypermotility in rats.

The model of LSD potentiated apomorphine hypermotility [5] was used to classify different atypical antidepressants (danitracen, mianserin, cyproheptadine) and pizotifen. All drugs have been shown to inhibit specifically the locomotor activity potentiating effect of LSD in a low dosage range (0.1-0.5 mg/kg i. p.) without influencing the apomorphine effect. Since there is some evidence that the effect of LSD is due to the inhibition of the activity of serotonergic raphe neurons, the marked antagonizing effects of danitracen, mainserin, cyproheptadine and pizotifen are regarded to be an expression of pronounced antiserotonin activity.

Animals↗
PubMed1980

Scopolamine-induced hypermotility in rats is mediated via a dopaminergic system.

To clarify the relation between cholinergic and dopaminergic transmission systems involved in locomotor effects the influence of dopaminergic drugs on scopolamine hypermotility was investigated. Scopolamine and apomorphine in locomotor stimulant doses showed additive effects. Apomorphine in a dose acting on presynaptic dopaminergic receptors decreased the scopolamine hypermotility markedly. Haloperidol antagonized both scopolamine and apomorphine hypermotility in an apparently competitive way. Sulpiride potentiated scopolamine locomotor effect. Additionally, it was shown that LSD potentiated scopolamine hypermotility as well as apomorphine hypermotility. The results suggest in connection with literature data that locomotor effects of drugs affecting cholinergic transmission may by mediated by a dopaminergic system.

Animals↗
PubMed1980

Kainic acid induced lesion of ventral tegmental area: locomotor effect of apomorphine.

Kainic acid induced lesion of dopaminergic ventral tegmental area (KA-A10) result in a permanent behavioral syndrome in the rat in which locomotor hyperactivity is the most typical symptom. Apomorphine in low doses (0.125 and 0.25 mg/kg i.p.) was as active as haloperidol (0.25 mg/kg i.p.) in abolishing this locomotor hyperactivity while higher doses of apomorphine were less active. The KA-A10 lesion is discussed as a model of mesolimbic/mesocortical dopaminergic hyperactivity.

Animals↗
PubMed1980

[Analysis of acetylcholine turnover in small brain areas in the rat with a two-compartment model].

A two-compartment model was used to calculate the turnover of acetylcholine in the Tuberculum olfactorium and the Nucleus accumbens septi. Radioactivity of [3H]-acetylcholine and [3H]-choline was measured in the areas after pulse injection of [3H]-choline. Acetylcholine and choline were determined radioenzymatically. The time dependence of specific activity of both choline and acetylcholine pools was calculated with an exponential polynomial function on a 9825A desk computer (Hewlett Packard). From the parameters of these functions a compartment analysis was performed. It was possible to determine the acetylcholine turnover exactly only if the analysis was perfomed from the acetylcholine pool (compartment B). The data of our model are discussed in relation to the literature.

Acetylcholine↗
PubMed1979

Psychotomimetics potentiate locomotor hyperactivity induced by dopaminergic drugs.

The spontaneous locomotor activity of rats was investigated in an open-field test. Apomorphine and d,1-amphetamine caused a dose dependent increase of locomotor activity. LSD, mescaline, and DMT in low doses were ineffective, when given alone, but caused a strong potentiation of the hypermotility induced by apomorphine and d,1-amphetamine. Cyproheptadine antagonized the potentiating effect of LSD without affecting the hypermotility induced by apomorphine, indicating a causal serotonergic involvement in the potentiation effect.

Amphetamine↗
PubMed1976

Studies on the loss of sensitivity in smooth muscle.

Specificity of desensitization effect was investigated at guinea pig ileum using the desensitizing agonists acetylcholine, carbachol, histamine, and serotonine. The desensitization with acetylcholine markedly diminished the contraction effects to test doses of all tested agonists. Contrary to acetylcholine, the histamine desensitization is mainly specific, the serotonine desensitization is a complete specific effect. A different influence of the tested agonists on intracellular ions is discussed.

Acetylcholine↗