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Biomedical subjects

J Maj

Publications and source records attributed to J Maj.

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

Desipramine given repeatedly enhances behavioural effects of dopamine and d-amphetamine injected into the nucleus accumbens.

The effect of desipramine (DMI) was studied after its repeated administration (10 mg/kg p.o., twice daily, 14 days) to rats, on the action of dopamine and d-amphetamine injected bilaterally into the nucleus accumbens. DMI, applied repeatedly but not acutely, prevented the sedative effect of dopamine and enhanced its stimulating action, as assessed by the open-field test. Repeated administration of DMI also enhanced d-amphetamine-induced locomotor hyperactivity. The number of [3H]SCH 23390 binding sites (D-1) in the limbic system decreased while the number of [3H] spiperone ones (D-2) remained unchanged. The results indicate that, like other antidepressant drugs studied earlier, DMI enhances neurotransmission in the dopamine mesolimbic system (nucleus accumbens) of the rat.

Animals↗
PubMed1987

Dihydropyridine calcium channel antagonists reduce immobility in the mouse behavioral despair test; antidepressants facilitate nifedipine action.

The effect of the calcium channel antagonists nifedipine, nitrendipine, nimodipine, verapamil and diltiazem in the mouse behavioral despair test was investigated. The dihydropyridine calcium channel antagonists nifedipine, nitrendipine, nimodipine (0.1, 1, 10 mg/kg p.o.) but not the non-dihydropyridine compounds verapamil or diltiazem, dose dependently reduced immobility. Various antidepressant drugs (imipramine, mianserin, citalopram, (+)oxaprotiline) and (-)oxaprotiline in combination with nifedipine facilitated its effect.

Animals↗
PubMed1987

Central action of ipsapirone, a new anxiolytic drug, on serotoninergic, noradrenergic and dopaminergic functions.

Ipsapirone (TVX Q 7821, 2-(4-(4-(2-pyrimidinyl)-1-piperazinyl)butyl)-1,2-benzisothiazol-3- (2H)one-1, 1-dioxidehydrochloride), a new anxiolytic drug in respect of the evaluation of its effect on central 5-hydroxytryptamine (5-HT), noradrenaline and dopamine functions was studied. It was found that ipsapirone inhibits induced by 8-OH-DPAT and 5-methoxydimethyltryptamine (agonists of 5-HT1A receptors) behavioural effects (flat body posture and forepaw treading) in normal and reserpinized rats. Ipsapirone partly inhibited in rats but not in mice the 8-OH-DPAT-induced hypothermia. Ipsapirone, administered at high doses, decreased the body temperature in rats and mice, inhibited the 5-hydroxytryptophan-induced head twitches in mice and the tryptamine-induced convulsions and tremor in rats. In the hind limb flexor reflex preparation of the spinal rat only high doses of the drug inhibited stimulation induced by quipazine, m-chlorphenylpiperazine, 8-OH-DPAT and St 587 (an agonist of alpha 1-adrenoceptors). Ipsapirone did not block the fenfluramine- and m-chlorphenylpiperazine-induced hyperthermia in rats at an ambient temperature of 28 degrees C. The drug did not affect clonidine-induced sedation and inconsiderably attenuated clonidine-induced hypothermia in mice. It attenuated the d-amphetamine-induced locomotor hyperactivity in mice and rats but, given alone, decreased the locomotor activity. The obtained results indicate that ipsapirone exhibits 5-HT1A antagonistic effect, and only at high doses it can also produce an inhibitory effect on 5-HT2 and the alpha 1-adrenergic function.

Animals↗
PubMed1987

Pharmacological properties of EXP 561, a potential antidepressant drug.

The compound EXP 561 (1-amino-4-phenylbicyclo-[2,2,2]-octane), an inhibitor of the noradrenaline (NA), 5-hydroxytryptamine (5-HT) and dopamine (DA) uptake, a potential antidepressant agent, was studied in tests for evaluation of antidepressant drugs (AD). In most experiments (the apomorphine and reserpine hypothermia, the behavioural despair test, the blood pressure increases induced by NA and 5-HT) EXP 561 revealed similar activities as tricyclic AD. EXP 561 evoked stimulation of the hind limb flexor reflex in spinal rats, blocked by prazosin, metergoline and clomipramine. EXP 561 administered repeatedly in mice (twice daily for 14 days) did not evoke the adaptive changes induced by AD inhibiting the amine uptake, i.e. it did not enhance the amphetamine locomotor hyperactivity, did not potentiate the clonidine aggressiveness (at a lower dose, while at a higher one it acted less potently than when given acutely) or did not change the reserpine effect on the locomotor activity. EXP 561 showed a poor affinity to alpha 1-adrenoceptor (IC50 was 135,000 nM). The results indicate that the inability to induce adaptive changes is a feature which differentiates EXP 561 from tricyclic AD.

Aggression↗
PubMed1986

Central action of the antidepressant drug pirlindole.

The central action of 2,3,3a,4,5,6-hexahydro-8-methyl-1H-pyrazino[3,2,1-j,k]carbazole hydrochloride (pirlindole, PIR) in mice and rats was studied. PIR inhibited the 3H-5-hydroxytryptamine (5-HT) uptake in the rat cerebral cortex, not affecting the uptake of 3H-noradrenaline. PIR counteracted the reserpine ptosis but did not alter the apomorphine hypothermia. It enhanced the L-dopa effect on the locomotor activity and the L-5-hydroxytryptophan (L-5-HTP)-induced head twitch reaction in mice. PIR also facilitated the effect of L-dopa and L-5-HTP on the hind limb flexor reflex of the spinal rat. The clonidine sedation (but not hypothermia) was attenuated by PIR. PIR given repeatedly for 18 days increased the binding of 3H-prazosin in the brain cortex (decreasing the KD value), but did not affect the binding of 3H-dihydroalprenolol. The obtained results indicate that PIR inhibits the 5-HT uptake, displays characteristics of a monoamineoxidase inhibitor and, when given repeatedly, increases the binding to alpha 1-adrenoceptors in the cerebral cortex.

5-Hydroxytryptophan↗
PubMed1985

Antidepressant drugs given repeatedly increase binding to alpha 1-adrenoceptors in the rat cortex.

The effect of antidepressant drugs, administered repeatedly, on binding to alpha 1-adrenoceptors in the rat cerebral cortex was studied using [3H]prazosin as a ligand. Imipramine, amitriptyline, citalopram and mianserin increased the binding (Bmax) assessed at 8:00 h. At 20:00 h such an effect was produced by imipramine, citalopram and mianserin. [3H]Prazosin binding in control rats was higher at 20:00 h than at 8:00 h. An increase in the density of alpha 1-adrenoceptors may be associated with the therapeutic activity of antidepressant drugs.

Animals↗
PubMed1985

Repeated treatment with imipramine potentiates the locomotor effect of apomorphine administered into the hippocampus in rats.

The effect of apomorphine, injected into the dorsal hippocampus, on the locomotor activity of imipramine-treated rats was studied. The rats were chronically implanted with cannulae 1 week before imipramine treatment. Imipramine was given in a dose of 10 mg/kg per os, acutely, or twice a day for 14 days. Intrahippocampal injection of apomorphine induced a dose-dependent increase in locomotor activity. This effect was antagonized by pretreatment with pimozide (2 mg/kg). Repeated, but not single, administrations of imipramine significantly enhanced the apomorphine-induced locomotor hyperactivity in rats. This effect was observed at 2, 48 and 96 h after the last dose of imipramine. The results obtained indicate that repeated administration of imipramine increases the responsiveness of the hippocampal dopaminergic system.

Animals↗
PubMed1985

Repeated treatment with imipramine or amitriptyline increases the locomotor response of rats to (+)-amphetamine given into the nucleus accumbens.

Effects of bilateral injections of (+)-amphetamine (5 micrograms/0.5 microliter) into the nucleus accumbens were investigated in rats treated repeatedly with imipramine or amitriptyline. Repeated but not acute administration of either drug enhanced the locomotor hyperactivity induced by (+)-amphetamine given 2 or 72 h after the last dose of antidepressant. The results indicate that the increased responsiveness of the mesolimbic dopaminergic system may be involved in the action of antidepressant drugs.

Amitriptyline↗
PubMed1984

Repeated treatment with antidepressant drugs increases the behavioural response to apomorphine.

The effect of repeated treatment (twice a day for 14 days) with antidepressant drugs (AD): imipramine, amitriptyline, zimelidine, citalopram and mianserin on the behavioural response to apomorphine in rats (open field test) was investigated. AD studied, given alone in a single dose or repeatedly, do not change the rats behaviour. A repeated but not single-dose treatment with AD facilitates the behaviour stimulation induced by apomorphine. This facilitation is observed 2 hours after the last dose of imipramine, zimelidine, citalopram and mianserin but 72 hours after the last dose of amitriptyline. The results presented suggest that the AD given repeatedly are able to increase the responsiveness of the brain DA system, probably the mesolimbic one.

Amitriptyline↗