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Biomedical subjects

S Ueki

Publications and source records attributed to S Ueki.

At least 253 records · Page 14Linked to original sources
PubMed1975

[Effects of various psychotropic drugs on self-stimulation behavior in the rat].

Effects of various psychotropic drugs on tegmental and hypothalamic self-stimulation behavior in rats with chronically implanted electrodes in the brain were studied. Effects of elecrtical stimulation in several brain structures on self-stimulation behavior and influences of drugs on the stimulation effect were also investigated. The hypothalamic self-stimulation behavior was more markedly inhibited by chlorpromazine than the tegmental self-stimulation, whereas the latter was more strongly inhibited by diazepam. The effects of pentobarbital on the self-stimulation behavior were similar to those of diazepam. Methamphetamine facilitated both the tegmental and hypothalamic self-stimulation behavior. Suppressive effect of hypothalamic stimulation on the tegmental self-stimulation behavior was inhibed by chlorpromazine, while those of amygdaloid and septal stimulation were augmented. All the effects of hypothalamic, amygdaloid and septal stimulating on the tegmental self-stimulation behavior were inhibed by diazepam and pentobarbital, while these were facilitated by methamphetamine. Suppressive effects of tegmental, amygdaloid and septal stimulation on the hypothalamic self-stimulation behavior were all facilitated by both chlorpromazine and methamphetamine. The effects of amygdaloid and septal stimulation on this behavior were inhibed by diazepam and pentobarbital, while those of tegmental stimulation were enhanced. The effects of imipramine, in all experiments, were variable in each rat and not significant.

Animals↗
PubMed1975

[Behavior pharmacology of maprotiline, a new antidepressant].

The effect of maprotiline (N-methyl-9, 10-ethanoanthracene-9 (10H)-propylamine) on animal behavior was investigated in mice and rats and compared with those of amitriptyline and imipramine. Maprotiline inhibited reserpine hypothermia in mice and tetrabenazine ptosis in rats, while it potentiated the effects of methamphetamine, L-DOPA and apomorphine in mice, in a similar manner to that of amitriptyline and imipramine. Maprotiline was more potent than anitriptyline and imipramine in antagonizing haloperidol-induced catalepsy as well as in suppressing muricide induced by either olfactory bulbectomy or delta-9-tetrahydrocannabinol in rats. Maprotiline potentiated anesthesia induced by thiopental or ether in mice to a lesser degree than did amitriptyline, and failed to counteract the lethal effect of physostigmine or oxotremorine tremor in mice, indicating that this drug has no central anti-cholinergic effect. Maprotiline markedly inhibited hyperemotionality of the rat with either septal lesions or olfactory bulb ablations, suggesting that it does have a tranquilizing effect. Inhibition of conditioned avoidance response of the rat in the shuttle box and reduction of methamphetamine group toxicity with maprotiline were similar to those with amitriptyline. Maprotiline exaggerated pentetrazol convulsion, decreased muscle tone and impaired coordinated motor activity in mice to a much lesser degree than amitriptyline and imipramine. LD50 of maprotiline was approximately twice that of imipramine and three times that of amitriptyline. These results indicate that maprotiline is a new type of antidepressant, has a low toxicity and shares both potent antidepressant and some tranquilizing effect, without possessing central anticholinergic action.

Aggression↗