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Biomedical subjects

J Vetulani

Publications and source records attributed to J Vetulani.

At least 73 records · Page 4Linked to original sources
PubMed1987

Antihistaminics enhance morphine-, but not amphetamine- and scopolamine-induced hyperactivity in mice.

Three histamine H1-receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine, were tested alone or in combination with morphine, amphetamine and scopolamine on locomotor activity in mice. All three antihistaminics, at some dosage levels, enhanced morphine-induced hyperactivity, but did not change or even reduce locomotor stimulation induced by amphetamine and scopolamine. The results suggest that H1-blocking agents may specifically interact, though not necessarily directly, with opiate mechanisms in producing behavioural effects.

Animals↗
PubMed1987

The effect of chronic imipramine and electroconvulsive shock treatment on [3H]DADLE binding to cortical membranes of rats pretreated with chronic reserpine or 6-hydroxydopamine.

Repetitive electroconvulsive shock treatment (for 8 days) or chronic administration of imipramine (10 mg/kg/day IP for 14 or 21 days) elevated the density of opioid delta receptors in the cerebral cortex of the rat. Electroconvulsive shock treatment produced a similar effect in rats treated subchronically with reserpine or receiving intraventricularly 6-hydroxydopamine, but these manipulations of central catecholamines prevented the action of imipramine.

Animals↗
PubMed1986

Effects of chronically administered antidepressants and electroconvulsive treatment on cerebral neurotransmitter receptors in rodents with 'model depression'.

The aim of this study was to develop a model of depression in laboratory animals in which chronically administered antidepressant drugs and electroconvulsive treatment (ECT) would produce receptor effects similar to but more marked than those in normal animals. The models discussed in detail are reserpinized and centrally chemosympathectomized rats. Other models currently under investigation are albino Swiss mice that respond with motor inhibition to high doses of morphine and rats tolerant to morphine. The reserpine model seems to be of some value, because in reserpinized rats antidepressants and ECT lead to adrenoceptor changes the same as or more marked than those observed in normal animals. Central chemosympathectomy with 6-hydroxydopamine prevents several receptor actions of imipramine, though not of ECT. The 'opiate models', though apparently not very promising, need further study.

Animals↗
PubMed1986

Facilitation of stimulatory effect of chlordiazepoxide-amphetamine combination by subacute administration of chlordiazepoxide in mice.

Spontaneous locomotor activity was tested in CD-1 mice receiving subacutely (for 4 days) chlordiazepoxide (10 mg/kg) and then treated with d-amphetamine (0.5 or 1 mg/kg) and various doses of chlordiazepoxide (2.5, 5 or 10 mg/kg) separately or in combination. Chlordiazepoxide pretreatment enhanced the stimulatory effect of the chlordiazepoxide-amphetamine combination.

Animals↗
PubMed1985

Chronic treatment with the potential antidepressant drug rolipram: the effect on the behavioural responses to adrenergic and dopaminergic receptor agonists with some biochemical correlates.

We studied the effect of acute and chronic treatment with rolipram, a potential antidepressant drug, on the behavioural responses induced by adrenergic and dopaminergic receptor agonists in mice and rats, and on (3H)prazosin and (3H)dihydroalprenolol binding to cortical membranes and whole brain noradrenaline and dopamine utilization in rats. Chronic, but not acute, administration of rolipram potentiated a behavioural response mediated through central alpha 1-adrenoceptors, attenuated an alpha 2-adrenoceptor-mediated response and inhibited a beta-adrenoceptor-mediated response. Neither treatment affected the behavioural responses to dopaminergic stimulants. Repeated treatment with rolipram decreased the density of cortical (3H)dihydroalprenolol, but not (3H)prazosin bindings sites, and reduced brain noradrenaline, but not dopamine utilization. These results suggest that chronic administration of rolipram induces the down-regulation of the central beta- and alpha 2-adrenoceptors and enhances the responsiveness of the central alpha 1-adrenoceptors with no apparent changes in the alpha 1-adrenoceptor density.

Aggression↗
PubMed1985

The role of trazodone metabolism in its inhibitory action on avoidance response.

To assess the role of trazodone metabolism in its depressant action on conditioned avoidance response we investigated whether in the mouse brain 3-chlorophenylpiperazine (CPP) is formed from trazodone, whether trazodone metabolism is affected by a drug metabolism inhibitor, proadifen, and how trazodone, CPP and their combinations act on avoidance responses in proadifen-pretreated mice. It was found that CPP is formed from trazodone in mice, that proadifen inhibits trazodone metabolism, and that the moderate and transient inhibitory effect of trazodone on avoidance responses is dramatically potentiated and prolonged in proadifen-pretreated mice. This effect, and inhibition of unconditioned escape response observed in mice receiving lower doses of trazodone after proadifen pretreatment, were counteracted by CPP. The results indicate that the inhibitory action of trazodone on avoidance response is caused by the parent compound, and that it is brief and moderate because of the rapid metabolism of the drug with formation of CPP which counteracts the depressant effect of the parent compound.

Animals↗
PubMed1985

Pharmacokinetics of morphine in striatum and nucleus accumbens: relationship to pharmacological actions.

The pharmacokinetics of morphine was compared with its ability to increase striatal dopamine turnover (estimated by an increase in DOPAC concentration) and to produce the development of a muscular rigidity (estimated as a tonic activity in the electromyogram). After systemic administration of morphine (15 mg/kg IP), the concentration of morphine in blood plasma, striatum and substantia nigra showed a parallel time course with a maximum after 30 min; in the striatum, in addition, normorphine was found in a lower concentration, but with a similar time course. The elevation of striatal DOPAC, in contrast, commenced very rapidly and lasted for about four hours. The rigidity appeared later and disappeared earlier than the striatal DOPAC elevation. After unilateral intrastriatal injection of morphine (15 micrograms), a small amount of the drug penetrated very rapidly to distant sites, such as the contralateral striatum and nucleus accumbens, as well as to the ipsilateral nucleus accumbens. The results suggest that the relationship between pharmacokinetics and pharmacodynamics of morphine, both after systemic and after local injection into the brain, is more complex than could be expected from previous findings.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Prolongation of thiopentone-induced sleep by trazodone and its metabolite, m-chlorophenylpiperazine.

Trazodone and its metabolite, m-chlorophenylpiperazine (CPP) prolonged significantly thiopentone-induced sleep in mice. Neither trazodone, nor CPP changed the cerebral concentrations of thiopentone. As cyproheptadine by itself did not affect thiopentone sleep and did not antagonize the effect of CPP, the effect of trazodone and CPP seems to be independent of their respective 5-HT-antagonistic and 5-HT-agonistic properties.

Anesthesia↗
PubMed1984

Opioid-specific recognition sites of the mu- and the delta-type in rat striatum after lesions with kainic acid.

The binding of 3H-dihydromorphine (3H-DHM) and of 3H-D-ala2, D-leu5-enkephalin (3H-DADL), which are regarded as relatively selective ligands for mu- or delta-type opioid receptors, respectively, was estimated in total particulate fraction of the striatum of rats in vitro, either in tissue of rats after striatal chemolesions with kainic acid or in control rats (not operated or saline injected into the striatum). Kainate lesions reduced the Bmax values of 3H-DHM by about 78 - 88% depending on the method of calculation, and of 3H-DADL by greater than 90%. Furthermore they lowered the Kd-values, suggesting an increase in affinity. The results are discussed with regard to recent hypotheses on the structure and function of opioid receptors.

Animals↗
PubMed1984

Electroshock-induced increase in [3H]prazosin binding to cortical membranes in reserpinized rats.

Chronic, spaced electroconvulsive shock (ECS, 6 treatments at 72 h intervals) produced a moderate (16%) increase in the density of [3H]prazosin binding sites to rat cerebral cortical membranes. The increase was of borderline significance (0.1 greater than P greater than 0.05) and KD was not affected. The effect was similar but much more pronounced (increase in Bmax by 38%, P less than 0.01) in rats receiving reserpine pretreatment (4 mg/kg i.p.) 24 h before each ECS. Reserpine produced a transient increase in [3H]prazosin binding 24 h but not 48 h after the last dose, at the time when the ECT effect was measured.

Animals↗
PubMed1984

Opposite action of m-chlorophenylpiperazine on avoidance depression induced by trazodone and pimozide in CD-1 mice.

m-Chlorophenylpiperazine (CPP) given in doses up to 2 mg/kg did not affect conditioned avoidance responses (CAR) of CD-1 mice pre-trained in a shuttle box. It reversed the inhibitory action of trazodone (10 mg/kg) on CAR, but dose-dependently potentiated the inhibitory effect of pimozide (0.2 and 0.5 mg/kg). Apparently, dopaminergic transmission is important for the attenuating effect of CPP on CAR inhibition.

Animals↗
PubMed1984

Effect of electroconvulsive treatment on cerebral opioid receptors in the rat: changes in delta but not mu receptors.

The rats subjected to repetitive electroconvulsive treatment (ECT; 8 electroshocks within 9 days) the density of specific 3H-D-Ala2, D-Leu5-enkephalin (3H-DADLE) binding sites in the cortical membranes was enhanced by approx. 60%, while the density of specific 3H-naloxone binding sites remained unchanged. In the striatum of rats subjected to ECT the specific binding of 3H-DADLE was reduced by 15%, and no change in 3H-naloxone binding was observed. The density of specific binding sites for either radioligand in the rest of brain remained unaffected by ECT. The results suggest that ECT affects specifically the opioid delta receptors in some brain areas.

Animals↗
PubMed1984

Complex action of antidepressant treatment on central adrenergic system: possible relevance to clinical effects.

Chronic antidepressant treatment with classical and atypical antidepressant drugs and ECT leads to complex changes in the central adrenergic system, consisting of upregulation of alpha 1 and downregulation of alpha 2 and beta adrenoceptors. These changes may lead to a specific facilitation of neurotransmission in structures employing alpha 1 adrenoceptors, involved in the control of mood and emotions.

Antidepressive Agents↗