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Biomedical subjects

J Vetulani

Publications and source records attributed to J Vetulani.

At least 91 records · Page 5Linked to original sources
PubMed1983

Chronic electroconvulsive treatment enhances the density of [3H]prazosin binding sites in the central nervous system of the rat.

Chronic electroconvulsive treatment (ECT) given daily for 10 days enhanced the density of [3H]prazosin binding sites in the membranes from the spinal cord and cerebral cortex of the rat 24 h after the last shock. Similar effect (investigated only in cortical membranes) was produced by spaced ECT (5 shocks at 72 h intervals). The effect was preceded by a decrease in the density of [3H]prazosin binding sites, observed 2 h after the last shock and disappeared within 48 h.

Animals↗
PubMed1983

Facilitation by alpha-adrenolytics of apomorphine gnawing behavior: depression of threshold apomorphine concentration in the striatum of the rat.

Adrenolytics, aceperone and phenoxybenzamine, increased significantly the incidence of gnawing induced in the rat by a medium dose of apomorphine. The experiments in which the rats were killed at the onset of stereotyped gnawing to assess the threshold concentration of apomorphine in the striatum necessary to evoke this type of behavior have shown that these threshold concentrations were significantly reduced. It is concluded that the facilitation by adrenolytics of gnawing response to apomorphine is caused by an increase in the sensitivity of structures involved in this phenomenon to this dopaminergic stimulant.

Animals↗
PubMed1983

Changes in morphine pharmacokinetics in nervous and peripheral tissues following different schedules of administration.

The pharmacokinetics of morphine were studied in various tissues of rats subjected to a single dose treatment (SDT, 30 mg/kg), constant dose treatment (CDT, 30 mg/kg daily for 8 days) and increasing dose treatment (IDT, twice daily, raising from an initial dose 20 mg/kg to the final 300 mg/kg). After CDT the elimination of morphine was slow and the drug was present in tissues in detectable amounts for over 24 hr, the area under the curve (AUC) values in the central nervous system increased significantly as compared with SDT. After IDT the elimination of morphine was rapid and the AUC values were decreased several times; in most of the tissues no detectable amount of morphine was present 24 hr after the last dose. The data indicate that morphine pharmacokinetics change after chronic treatment and depend on dosage schedule and that plasma concentration of morphine may not reflect the drug level in tissues, particularly in the central nervous system.

Animals↗
PubMed1982

Postdecapitation convulsions in the rat measured with an Animex motility meter: relation to central alpha-adrenoceptors.

Postdecapitation convulsions (PDC) were quantified by recording the number of movements of the trunk of decapitated rats with an Animex motility meter. PDC were inhibited by alpha 1-adrenoceptor blocking agents, phenoxybenzamine and prazosin, but unaffected by alpha 2-adrenoceptor antagonists, yohimbine and piperoxan, or a beta-adrenoceptor blocker, propranolol. Chronic administration of antidepressant drugs: amitriptyline, imipramine and zimelidine augmented the PDC. Preliminary experiments with [3H]prazosin binding suggest that the increased PDC response is related to an increase in alpha 1-adrenoceptor binding, most likely owing to an increase in receptor density.

Adrenergic alpha-Antagonists↗
PubMed1982

Depression by chronic electroconvulsive treatment of clonidine hypotherma and [3H]clonidine binding to rat cortical membranes.

The effects of chronic electroconvulsive treatment (ECT) on the binding of [3H]clonidine and on clonidine-induced hypothermia were studied in the rat. After 10 consecutive daily treatments we observed a reduction in the hypothermic action of clonidine and a loss of the high affinity binding sites of clonidine, without changes of the low affinity binding sites. The present results are indicative of the down-regulation of alpha 2-adrenoceptors during chronic antidepressive treatment.

Animals↗
PubMed1982

Attenuation by chronic imipramine treatment of [3H]clonidine binding to cortical membranes and of clonidine-induced hypothermia: the influence of central chemosympathectomy.

Central chemosympathectomy with intraventricular injection of 250 microgram of 6-hydroxydopamine, resulting in depression of cerebral noradrenaline level by 75% led to an increase in specific binding of [3H]clonidine to cerebral cortical membranes, but did not affect the hypothermic response to clonidine. Chronic imipramine treatment depressed [3H]clonidine binding and attenuated clonidine-induced hypothermia similarly in non-chemosympathectomized and chemosympathectomized rats.

Animals↗
PubMed1982

Different effects of 3-chlorophenylpiperazine on locomotor activity and acquisition of conditioned avoidance response in different strains of mice.

Mice of C57BL/6 (C57), Balb/c (BALB), and CD-1 (CD) strains were injected with 3-chlorophenylpiperazine (CPP), 1-10 mg/kg ip, and their exploratory and basal locomotor activities and acquisition of conditioned avoidance response in a shuttle-box were tested. In C57 mice CPP did not affect either locomotor activity or shuttle-box performance. In BALB mice CPP inhibited both basal and exploratory activities (the latter only in higher doses) and facilitated the acquisition of conditioned avoidance response. In CD mice CPP did not affect exploration, but inhibited basal locomotor activity and facilitated the shuttle-box performance. It is concluded that there exist large interstrain differences in responsiveness of mice to CPP, and that the drug may facilitate acquisition of conditioned avoidance response through a strain-specific, serotonin-independent mechanism.

Animals↗
PubMed1982

Cataleptogenic doses of morphine suppress 3H-spiroperidol binding to striatal membranes.

The Scatchard analysis of 3H-spiroperidol binding to crude synaptosomal fraction of rat striatum has revealed that in rats receiving cataleptogenic doses of morphine the density, but not affinity of dopamine receptor is depressed. The effect is mediated through opiate receptor, as it is reversible with naloxone. The data support the idea that one population of receptors may regulate another receptor population, and may explain the mechanism of morphine-induced catalepsy and increase in striatal dopamine turnover.

Animals↗
PubMed1982

Dopamine receptors in the striatum and limbic system of various strains of mice: relation to differences in responses to apomorphine.

Dopamine receptors, defined as [3H]spiroperidol binding sites, had similar population parameters in the limbic forebrain of C57BL/6, Albino Swiss and DBA/2 mice, but the parameters of the striatal populations were different: not only the densities differed among themselves, but the KD value of the striatal dopamine receptors of DBA/2 mice was significantly higher than that in the two remaining strains. Behavioral responses of Albino Swiss mice to apomorphine: biphasic effect of apomorphine on locomotor activity and stereotypy characterized by high motility, frequent rearing and sharp, not very frequent bites, were similar to those described earlier for C57BL/6 mice, and differed from those reported for DBA/2 mice. The results suggest that the difference in responding to apomorphine in various strains of mice may be related to differences in their striatal dopamine receptors.

Animals↗
PubMed1982

Analysis of the difference in the behavioral effects of apomorphine in C57BL/6 and DBA/2 mice.

The influence of pimozide on the effects of apomorphine on locomotor activity and stereotypy was studied in two inbred strains of mice. In C57BL/6 mice, in which apomorphine did not produce stereotypy of gnawing, the biphasic effect of apomorphine on locomotor activity (hypomotility followed by hypermotility) was unaffected by pimozide. In DBA/2 mice, in which high doses of apomorphine produce hypomotility and compulsive gnawing, both these effects (but not hypomotility produced by low doses of apomorphine) were counteracted by pimozide. The results are consistent with the assumption that both strains of mice have separate inhibitory and stimulatory dopamine receptors mediating locomotor activity. In addition, DBA/2 but not C57BL/6 mice have dopamine receptors which mediate stereotypy and are sensitive to pimozide.

Animals↗
PubMed1982

Central action of amitriptyline N-oxide.

The central action of amitriptyline N-oxide (AMINO) has been compared with amitriptyline (AMI) in biochemical and pharmacological studies in rats and mice. It has been found in rats that both drugs prevent 6-OH-dopamine-induced depletion of brain noradrenaline (NA). At the same time AMINO increases and AMI lowers the NA level, both being without effect on 3-methoxy-4-hydroxyphenylglycol concentrations in the brain. AMINO and AMI potentiate the depletion of 5-hydroxytryptamine (5-HT) induced by p-chloroamphetamine in the rat brain and it may be considered as evidence that both drugs do not inhibit 5-HT uptake in vivo. Neither AMINO nor AMI affects the rat brain level of 5-HT but at higher doses they elevate the 5-hydroxy-indoleacetic acid concentrations. AMINO antagonizes the head twitch reaction induced by 5-hydroxytryptophan in mice and tryptamine convulsions in rats. The hyperthermia induced by fenfluramine (in rats at a high ambient temperature) as well as the stimulation of the hind limb flexor reflex in spinal rats, induced by fenfluramine or LSD, are also inhibited. AMINO antagonizes the 5-HT-induced increase in blood pressure in pithed rats. All the above effects are similar to those induced by AMI, only the active doses of AMINO are higher. The results presented indicate that AMINO, like AMI, inhibits NA uptake and is a 5-HT antagonist.

5-Hydroxytryptophan↗
PubMed1982

3H-dihydromorphine binding sites in subcellular fractions of rat striatum.

Binding of low concentrations of 3H-dihydromorphine (3H-DHM) that label specifically opiate mu receptors was tested in the whole particulate (P1 + P2), P1 and P2 fractions of rat striatal homogenate. Two subpopulations of 3H-DHM binding sites were revealed by Scatchard analysis in the whole particulate and in P2 fractions: high-affinity sites of KD approx. 0.2 nM, and low-affinity sites of KD approx. 3 nM. In P1 fraction only one population of low-affinity binding sites was present. Assuming that opiate receptors are predominantly located on synaptosomal membranes, it may be concluded that only high affinity 3H-DMH binding sites represent opiate mu receptors.

Animals↗
PubMed1981

Enhancement of responsiveness of the central serotonergic system and serotonin-2 receptor density in rat frontal cortex by electroconvulsive treatment.

The effect of a series of 10 electroconvulsive shocks (ECS) on the hyperthermic response of heat-adapted rats to a serotonergic stimulant, 3-chlorophenylpiperazine (CPP), and on radioligand binding to serotonin-1 and serotonin-2 receptors in frontal cortical membranes was investigated. Chronic ECS augmented the hyperthermic response of rats to CPP, did not affect [3H]serotonin binding to serotonin-1 receptors, and increased [3H]spiroperidol binding to serotonin-2 receptors. The treatment increased the density of serotonin-2 receptors by about 40%. It is suggested that the increased responsiveness of the central serotonergic system may be an important factor in the antidepressant action of chronic ECS.

Animals↗