Stress-induced depression of basal motility: effects of antidepressant drugs.

Behavioral and biochemical effects of repeated immobilization stress were determined in male Wistar rats. The influence of acute or repeated administration of antidepressant drugs on these effects of stress were also evaluated. It was found that repeated stress (immobilization 3 h/2 degrees C/4 days or various stressors/8 days) reduced basal locomotor activity of rats and prolonged immobility time in Porsolt's despair test. Antidepressant drugs (desmethylimipramine, imipramine, amitriptyline, clomipramine, mianserine), given acutely, restored basal locomotor activity of stressed rats to control level. Desmethylimipramine, imipramine and amitriptyline reduced immobility time in Porsolt's test similarly in control as in stressed rats. However clomipramine, mianserine and trazodone were effective in this test only in stressed rats. Imipramine given for 4 or 8 days (1 h before the stressor) normalized basal locomotor activity. Repeated (for 8 days) various stressors decelerated utilization of noradrenaline (NA) and dopamine (DA) in the brain. Imipramine given once a day for 8 days (1 h before the stressor) normalized brain utilization of catecholamines (CA). It was proposed that depression of basal motility and reduction of CA utilization in the brain induced by repeated stress may be counter acted by antidepressant drugs.

Immobilization stress modifies locomotor response to catecholamine receptor agonists in rats.

The effects of dopaminergic (apomorphine, nomifensine, B-HT 920) and noradrenergic (methoxamine, clonidine, salbutamol) agonists on locomotor activity were investigated in rats submitted to acute (3 h) or repeated (3 h/4 days) immobilization stress. The stress-induced functional changes were monitored by the blood level of corticosterone and the number of lymphocytes as well as the brain utilization of NA and DA. The rats subjected to acute immobilization stress displayed 30 min later an enhanced locomotor activation after apomorphine, nomifensine, or methoxamine and reduced sedative effect of clonidine, salbutamol or B-HT 920. 24 h after the repeated stress only the locomotor responses to apomorphine, nomifensine, B-HT 920 and salbutamol were modified. Spontaneous locomotor activity was not significantly changed under the influence of stressful stimuli. Increased plasma corticosterone level, strong reduction of blood lymphocytes and enhanced NA and DA utilization in the brain of rats after acute stress, together with above mentioned results, suggest that short-lasting stress evokes (30 min later) significant functional changes not only in the blood but also in the brain: enhanced CA neurons activity as well as the increased alpha 1-adrenergic and DA-post-synaptic receptors responsiveness in parallel with reduced alpha 2 - and beta-adrenergic and DA-presynaptic receptors reactivity. On the other hand, 24 h after last session of repeated stress CA brain neurons activity was not changed, however DA and beta-adrenergic responsivity was farther modified. It is postulated that the stress conditions produce in NA and/or DA brain systems a state of readiness to locomotion activating stimuli.

Anticataleptic effect of taurine: interaction with antiparkinsonian agents.

The influence of taurine on cataleptogenic effect of neuroleptics was investigated in male Wistar rats. It was found that taurine 900 micrograms/rat icv reduced significantly haloperidol or fluphenazine-induced catalepsy. In rats receiving taurine in a dose of 450 micrograms, not influencing catalepsy, with low doses of anticholinergic antiparkinsonian agents (trihexyphenidyl and pridinol) strong anticataleptic effect was observed. The results suggest that taurine facilitates neurotransmission in nigrostriatal dopaminergic neurons.

Interaction of antidepressants with antiparkinsonian agents in rats.

The influence of antidepressants: nomifensine, imipramine, amitriptyline and trazodone on the effect of antiparkinsonian agents: trihexyphenidil and L-DOPA + carbidopa mixture (sinemet) in the model of haloperidol catalepsy was investigated in rats. In some experiments deprenyl, a selective MAO-B inhibitor, was used. It was found that antidepressant drugs in doses not influencing haloperidol catalepsy enhanced significantly the anticataleptic effect of trihexyphenidil and L-DOPA + carbidopa. The most effective in the interaction with both antiparkinsonian agents was nomifensine. Imipramine and trazodone potentiated anticataleptic effect of L-DOPA + carbidopa more strongly than those of trihexyphenidil. The most potent anticataleptic effect was observed after combined treatment of rats with deprenyl and L-DOPA + carbidopa.