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Biomedical subjects

J Vetulani

Publications and source records attributed to J Vetulani.

At least 109 records · Page 6Linked to original sources
PubMed1981

Cerebral pharmacokinetics of imipramine in rats after single and multiple dosages.

Pharmacokinetics of imipramine (IMI) and its active metabolite, desipramine (DMI) was studied in rats after administration of a single dose of 10 mg/kg IMI, or after chronic administration of this dose once or twice a day for 14 days. The elimination curves of IMI and DMI from the blood and brain show that both the whole body and the brain behave as multi-compartment systems. Maximum concentrations of IMI and DMI in blood and brain appear at the same time, indicating rapid metabolism of IMI: the concentrations were significantly higher in the brain than in the blood. After the chronic treatment the maximum blood and cerebral levels of IMI and DMI were not much higher than after a single dose, but the elimination was slowed down. Brain concentration of IMI and DMI and brain IMI/DMI concentration ratio do not parallel those in the blood. After a prolonged treatment, once or twice a day, desipramine in the brain is present for the whole period between injections at concentrations sufficient to inhibit the noradrenaline uptake. If the drug is given twice a day, in addition to DMI also IMI is present for the whole time at concentration which may inhibit also serotonin uptake.

Animals↗
PubMed1981

The effect of drugs on accumulation of exogenous norepinephrine in nervous tissue cultured in vitro. IV. The effect of clonidine.

Explants of nervous tissue taken up from the area of locus coeruleus from rats 3-36 days old were cultured in vitro for 15 days, and than accumulation of norepinephrine (3 X 10-8M) was studied with and without preincubation with equimolar concentration of clonidine, using histofluorescence methods. Preincubation with clonidine increased the fluorescence in neural cells, particularly those derived from young animals, in which the pattern of fluorescence appeared to resemble the observed without preincubation only in cells from older animals in addition to fluorescence in the cells, fluorescent granules appeared in neuronal processes and in structures resembling non adrenergic nerve endings. Clonidine completely inhibited norepinephrine uptake by glial cells from very young animals, and inhibited that in the glia in colonies derived from 18-24 days old rats. However, clonidine preincubation restored accumulation of norepinephrine by oligodendroglia from 36 days old rats already lost by this age, but did not affect astrocytes.

Animals↗
PubMed1980

Motor depression and head twitches induced by IP injection of GABA.

Influence of GABA onlocomotor activity and gross behavior of mice, rats, and rabbits was studied. In mice and rats, IP GABA injection produced decreased locomotor activity, but in rats and rabbits head twitches and disturbances in body balance were seen. GABA-induced head twitches were inhibited by picrotoxin, clonidine, morphine, or cyproheptadine. Our results suggest a serotonergic component in GABA-induced head twitches, but it is not the only mechanism involved in this behavior.

Animals↗
PubMed1980

The effect of drugs on accumulation of exogenous norepinephrine by nervous tissue in vitro.

The effect of hydrocortisone and prednisone on accumulation of exogenous norepinephrine was tested in nervous tissue in vitro, taken from rats at various periods of the postnatal life. The results indicate that exogenous norepinephrine is taken up by either uptake1 or uptake2 or both, depending on the age of explant donors and the kind of the cell. Uptake1 appearing predominantly in the tissue from young animals, in first days of postnatal life, differs from the uptake2 in the cardiac muscle in that it is inhibited by hydrocortisone, inactive in this respect in the heart.

Aging↗
PubMed1979

Central dopamine receptors regulate blood eosinophilia in the rat.

Dopaminergic agents, dopa and apomorphine, affected biphasically the blood eosinophil count in the rat: low doses of the drug elevated, while high doses lowered it. The response to a high dose of dopa was retained in rats pretreated with an inhibitor of dopamine-beta-hydroxylase, U 10, 157, but prevented by a centrally acting dopa decarboxylase inhibitor, NSD 1015. This indicates that the eosinopenia observed after large doses of dopa is due to the action of dopamine formed from the precursor. As intracerebroventricular injections of Ldopa also produce eosinopenia, the central site of dopamine action is indicated. The eosinopenic response to apomorphine was antagonized by a dopamine receptor blocking agent, haloperidol. This indicates that some central dopamine receptors are involved in the regulation of the eosinophil count in circulating blood. The hypophysis seems to play a crucial role in the phenomenon observed, as no eosinopenia was produced by dopa in hypophysectomized rats.

Animals↗
PubMed1979

Accumulation of apomorphine in caudate nucleus and hippocampus of the rabbit.

Apomorphine concentration was assayed in the caudate nucleus, hippocampus and cerebellum of rabbits injected with various doses of the drug 30 min earlier. Apomorphine accumulation was dose-dependent but uneven in the structures tested: the accumulation in the caudate nucleus being approx. 5 times higher than in cerebellum. Pretreatment with haloperidol significantly depressed the accumulation of apomorphine in the caudate nucleus and hippocampus, but not in the cerebellum. The amount of apomorphine displaceable by haloperidol was approx. 10 times higher in the caudate nucleus than in the hippocampus. The results suggest the existence of small number of apomorphine binding sites in the hippocampus.

Animals↗
PubMed1978

Inhibition of "wet shakes" during morphine abstinence by an antagonist of opiate analgesia.

An antagonist of morphine analgesia, N-cyclopropylmethylnorazidomorphine (CAM) inhibited the"wet shakes" appearing during spontaneous or nalorphine-precipitated morphine abstinence. CAM inhibited the pinna reflex more strongly than did morphine and selectively antagonized quipazine-induced head twitches; its inhibition of head twitches induced by 5-hydroxytryptophan or LSD seemed unspecific. The results suggest that the opiate receptors involved in the inhibition of some symptoms of morphine abstinence and of the pinna reflex differ from those involved in opiate analgesia.

5-Hydroxytryptophan↗