Search PubMed⌕ Search

Biomedical subjects

J Maj

Publications and source records attributed to J Maj.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Effects of repeated treatment with antidepressant drugs on the 24 hour behavior in the light-dark synchronized mice.

Imipramine, amitriptyline, citalopram, zimelidine and mianserin--antidepressant drugs with a different mechanism of pharmacological activity, as well as haloperidol, a neuroleptic, and diazepam, an anxiolytic, administered for 14 days, were examined in photoresistor actometers in the exploratory activity test (within the first 60 min) and in the basic locomotor activity test (the following 11 h) in the light and dark phases of the LD 12:12 cycle. Imipramine had no effect on the exploratory activity in either phase of the cycle, yet it enhanced the basic locomotor activity in the light phase. Amitriptyline stimulated only the exploratory activity in the dark phase. Citalopram enhanced the exploratory activity in both phases and did not change the basic locomotor activity in either phase of the cycle. Zimelidine increased the exploratory activity in the dark phase and inhibited the basic locomotor activity in both phases. Mianserin stimulated the exploratory activity in the dark phase and the basic locomotor activity in the light one, yet it inhibited the latter in the dark phase. Haloperidol attenuated the exploratory activity in both phases and the basic locomotor activity in the light phase. Diazepam enhanced the exploratory activity in both phases, exerting no effect on the basic locomotor activity. The results indicate that the examined antidepressant drugs administered repeatedly exert a diversified effect on the exploratory activity and the basic locomotor activity in the dark and light phases, yet the dominating feature is the increased exploratory activity in the dark phase.

Animals↗
PubMedDate not supplied

The central action of carbamazepine as a potential antidepressant drug.

Carbamazepine (CBZ) was studied in mice and rats with regard to its antidepressant activity. CBZ did not counteract hypothermia and ptosis induced by reserpine, hypothermia evoked by apomorphine, or sedation and hypothermia induced by clonidine. CBZ shortened the immobility time in the behavioral despair test in rats (but not in mice). It attenuated hyperactivity evoked by d-amphetamine, not affecting stereotypy induced by that drug. CBZ inhibited head twitches evoked by 5-HTP, as well as the hind limb flexor reflex of the spinal rat, having no effect on its stimulation by noradrenaline and 5-hydroxytryptamine agonists. CBZ administered repeatedly did not enhance clonidine aggressiveness or d-amphetamine locomotor hyperactivity, acting differently than many antidepressant drugs. The obtained results indicate that CBZ is not similar in its action to typical and many atypical antidepressants.

Aggression↗
PubMedDate not supplied

On the central antiserotonin action of trazodone.

Trazodone, an antidepressant drug with an unknown mechanism of action, has been examined in order to demonstrate its central antiserotonin action. Trazodone antagonizes the head twitch response induced by 5-hydroxytryptophan in rats and mice, or by-5-methoxytryptamine in rats (the ED50 values are 9.3, 5.2, and 10.8 mg/kg respectively). It counteracts convulsions induced by tryptamine in rats (ED50=3.75 mg/kg). Trazodone abolishes hyperthermia induced by serotoninomimetics (LSD, quipazine, fenfluramine) in rabbits. It does not affect ptosis induced by reserpine, and diminishes stimulation of the locomotor activity induced by amphetamine. Our findings demonstrate that trazodone has a central antiserotonin action, similarly as three other antidepressant drugs: mianserin, danitracen and doxepin, whose central antiserotonin action has been found previously.

Animals↗
PubMedDate not supplied

Central effects following repeated treatment with antidepressant drugs.

The review sums up the results of experiments in which there were studied central effects following repeated administration of various antidepressant drugs (AD) in rats and mice. A number of typical and atypical AD, except for selective inhibitors of 5-hydroxytryptamine (5-HT) uptake, potentiate the clonidine aggressiveness in mice (medicated by alpha 1-adrenoceptors). These results indicate that the repeated AD administration enhances responsiveness of central postsynaptic alpha 1-adrenoceptors. This assumption is in accordance with electrophysiological literature data. A few AD (including citalopram, a selective inhibitor of the 5-HT uptake), administered repeatedly, potentiate the locomotor hyperactivity induced by D-amphetamine or apomorphine, without affecting the stereotypy evoked by both dopaminomimetics. It may be supposed that AD enhance the responsiveness of a dopamine (DA) system, probably the mesolimbic one (but not the striatal one). A repeated administration of various AD also counteracts the locomotor hypoactivity induced by salbutamol (mediated by a beta-adrenoceptor). The importance of the effects stated above (alpha 1 up-regulation, DA up-regulation, beta down-regulation) for the mechanism of antidepressant action has been discussed.

Aggression↗
PubMedDate not supplied

The effect of proadifen, a drug metabolism inhibitor, on action of imipramine and desipramine in mice.

Proadifen (SKF 524 A) inhibited the following effects of imipramine (IMI), without affecting those of desipramine (DMI) in mice: antagonism towards reserpine-induced hypothermia, ptosis and sedation, antagonism to apomorphine hypothermia and insignificant shortening of the immobility time in the behavioral despair test. Cerebral levels of DMI were very low after administration of IMI; pretreatment with proadifen did not affect the already low levels of DMI but significantly elevated these of IMI. This may indicate that some other than DMI metabolites (e.g., 2-hydroxy-derivatives) may be of importance for the action of IMI in mice in the tests employed in this study.

Animals↗