Search PubMed⌕ Search

Biomedical subjects

S Ueki

Publications and source records attributed to S Ueki.

At least 199 records · Page 11Linked to original sources

Effects of monoamines injected into the hippocampus on hippocampal seizure discharges in the rabbit.

The effects of intrahippocampally administered catechol- and indoleamines on the two types of hippocampal seizure discharges elicited by electrical and chemical stimulation were examined in unanesthetized rabbits. The catecholamines norepinephrine (NE) and dopamine (DA), injected into the hippocampus in doses of 100--200 micrograms, inhibited electrically induced hippocampal seizure discharges with a 50% increase in the stimulation threshold. However 5-hydroxytryptamine (5-HT) at doses of 50 micrograms to 100 micrograms caused no effect on electrically induced seizure discharges. On the contrary, 5-HT and 5-hydroxytryptophan (5-HTP) at a dose of 50 micrograms potentiated carbachol (5 micrograms)-induced hippocampal seizure discharges, prolonging the duration of seizure discharge three times the control. NE and DA had no effect on this chemically induced hippocampal discharges. It is therefore suggested that the effects of monoamines on hippocampal seizure discharges are very much dependent on the type of stimulation employed for the induction of this phenomenon.

Animals↗

Effects of electroconvulsive shock on mouse-killing behavior (muricide) in olfactory bulbectomized rats.

We investigated the influence of electroconvulsive shock (ECS), regarded to possess an antidepressant effect clinically, on muricide in olfactory bulbectomized rats (OB rats). Muricide in these rats was markedly inhibited by ECS treatment. Five and 10 min after the termination of ECS-induced convulsions, muricide was inhibited by 100%. Even after intervals of 20 and 60 min, inhibition rates of 80% and 30% were obtained, respectively. ECS-induced muricide inhibition was remarkably antagonized by pretreatment with the alpha-blocker phenoxybenzamine but not by pretreatment with the beta-blocker sotalol. ECS-induced suppression of muricide was potentiated by repeated ECS treatment once daily for 10 days. After several applications of ECS treatment, muricide was inhibited in muricide tests done 24 hours after ECS treatment; this state persisted for up to 10 days thereafter. The results of this experiment demonstrated that ECS treatment specifically inhibited muricide in OB rats and further suggested that the cerebral noradrenergic alpha-receptor system plays an important role in this ECS-induced inhibition of muricide. Similar findings in the case of antidepressant administration, inhibition of muricide was potentiated by chronic ECS treatment. Specific inhibition of muricide in OB rats by antidepressants indicated that this phenomenon may serve as an animal model for the evaluation of antidepressant activity. Our results reiterate the usefulness of muricide in OB rats as an excellent experimental model for the assessment of antidepressant activity.

Aggression↗

[Behavioral and electroencephalographic effects of alprazolam and its metabolites (author's transl)].

The behavioral and electroencephalographic effects of alprazolam and its metabolites were investigated in mice, rats and rabbits, and compared with the data on diazepam, lorazepam and nitrazepam. Locomotor activity of mice in an open-field situation was increased with smaller doses of alprazolam and nitrazepam but not with diazepam and lorazepam. Alprazolam increased the hyperactivity induced by methamphetamine in mice. The anticonflict effects of alprazolam in rats were more potent than those of diazepam and lorazepam. In suppressing hyperemotionality and muricide of olfactory bulbectomized rats, alprazolam was more potent than diazepam and fairly equal to that of lorazepam. Muricide of raphe-lesioned rats was markedly inhibited by alprazolam. Mescaline-induced head-twitches in mice were more markedly increased with alprazolam than with nitrazepam and diazepam. Alprazolam, diazepam and lorazepam prevented both maximal electroshock and pentetrazol convulsions in mice. Alprazolam was more potent than diazepam and lorazepam in potentiating thiopental, ether and ethanol anesthesia in mice. In the impaired rotarod performance, alprazolam was more potent than diazepam and lorazepam in mice, but was much less potent than diazepam and lorazepam in mice, but was much less potent than lorazepam in rats. In conscious rabbits with chronically implanted electrodes, alprazolam induced a drowsy EEG pattern and depressed the EEG arousal response not only to auditory stimulation but also to mesencephalic reticular stimulation. The EEG effect of alprazolam was approx. twice that of diazepam. The pharmacological activity of alpha-hydroxyalprazolam was approx. one third that of alprazolam. However, 5-chloro-2-(3-hydromethyl-5-methyl-4H-1, 2,4-triazolo-4-yl) benzophenone showed no pharmacological activity. These results indicate that alprazolam possesses pharmacologic properties characteristic to benzodiazepines and that the activity is more potent than diazepam. In addition, alprazolam seems to have a specific effect on the central serotonergic mechanisms.

Aggression↗

Effects of chronic administration of delta 9-tetrahydrocannabinol on the cardiovascular system, and pressor and behavioral responses to brain stimulation in freely moving rats.

The effects of chronic administration of delta 9-THC on the cardiovascular system, and the pressor and behavioral responses to brain stimulation were investigated in freely moving rats with chronic electrode and arterial cannula implants. delta 9-THC at a dose of 6 mg/kg was injected intraperitoneally once a day for 10 days through an abdominal cannula. On the first day, delta 9-THC induced a significant decrease in heart rate and rise in blood pressure. The animals exhibited abnormal behavior such as catalepsy, walking backward and pivoting. On the 5th day, the bradycardia induced by delta 9-THC markedly decreased and on the 10th day tachycardia was observed. The pressor effect of delta 9-THC significantly increased on the 5th and 10th days. However, delta 9-THC-induced abnormal behavior was observed without any changes following chronic administration. delta 9-THC inhibited the pressor response and behavioral changes to electrical stimulation of the posterior hypothalamus and midbrain reticular formation. No tolerance developed to these depressive effects of delta 9-THC after chronic treatment. These data suggest that tolerance develops only to bradycardic effect of delta 9-THC and that the decrease in vagal activity may play some role in the development of tolerance.

Animals↗

Effects of psychotropic drugs on delta 9-tetrahydrocannabinol-induced long-lasting muricide.

The effects of psychotropic drugs on THC-induced long-lasting muricide were investigated in rats. Changes in open field activity (ambulation and rearing) of the rat were concurrently assessed as an index of behavioral toxicity. Imipramine-like antidepressants, atropine, and antiparkinsonism drugs exhibited a selective inhibitory activity on muricide, whereas the effects of neuroleptics, pentobarbital, diazepam, and methamphetamine were nonspecific. It is also suggested that cholinergic, catecholaminergic, and serotonergic mechanisms are involved in THC-induced muricide. This type of induced muricide appears to be a useful experimental model particularly suitable for the evaluation of antidepressants in correlation with brain amine dynamics.

Aggression↗

The effect of age on the development of hyperemotionality following bilateral olfactory bulbectomy in rats.

The effect of age on the development of hyperemotionality including muricide induced by either olfactory bulbectomy or isolated housing was studied in rats. In olfactory bulbectomized groups, 13-week-old rats showed the highest score of emotionality and shortest latency in the onset of hyperemotionality and muricide among any other groups of rats. On the other hand, in the groups subjected to isolation, 4-week-old rats showed a higher score of emotionality than 13-week-old rats. These results suggest that the age of the rat at the beginning of experiment is quite important in the induction of hyperemotionality following both olfactory bulbectomy and isolated housing.

Aging↗

Effects of limbic lesions, especially of olfactory bulbectomy on simple conditioned avoidance response in rats.

Effects of olfactory bulbectomy, and lesions of the septum and dorsal hippocampus on emotionality as well as on the simple conditioned avoidance response in a two-way shuttle box were investigated in rats. The rats with bilateral olfactory bulbectomy (O. B. rats) showed hyperactivity and aggressive behavior, including mouse-killing behavior (muricide), and those with septal lesions exhibited hyperreactivity and hypoactivity, while the rats with hippocampal lesions became hypoactive without showing hyperreactivity. The O. B. and septal rats, on an average, showed a facilitation in acquisition of the conditioned avoidance response and a retardation in extinction. The muricidal group of O. B. rats, however, showed slower acquisition, while the nonmuricidal O. B. rats showed much faster acquisition and slower extinction than intact rats. Hippocampal lesions retarded acquisition.

Aggression↗

Effects of delta-9-tetrahydrocannabinol on the cardiovascular system, and pressor and behavioral responses to brain stimulation in rats.

Effects of delta-9-tetrahydrocannabinol (delta 9-THC) on the cardiovascular system, and pressor and behavioral responses to brain stimulation were investigated in rats. In urethane-anesthetized rats, intravenous administration of delta 9-THC (1, 2 and 5 mg/kg) produced a significant and transient dose-related rise but no fall in blood pressure. delta 9-THC at these doses also produced marked reduction in heart rate which was antagonized by atropine (0.5 mg/kg i.v.) or bilateral vagotomy. In freely moving rats with chronically implanted electrodes and arterial cannula implants, intraperitoneal administration of delta 9-THC (4, 6 and 8 mg/kg) induced a rise in blood pressure and marked bradycardia. Abnormal behavior such as catalepsy, walking backwards and pivoting was also observed. delta 9-THC failed to inhibit the pressor responses to electrical stimulation of the posterior hypothalamus and midbrain reticular formation, whereas the drug suppressed the behavioral responses to stimulation of both regions. It is concluded that the cardiovascular effects seen with delta 9-THC injection are mainly the result of alteration of the efferent vagal activity by acting on the central nervous system and a more potent influence is exerted on the behavioral changes than on autonomic responses to brain stimulation.

Anesthesia↗

[Effects of quinazoline-2, 4(1H, 3H)-dione compound, H-88 and pyridopyrimidine-2, 4(1H, 3H)-dione compound, HN-37 on pituitary-adrenal axis in rats (author's transl)].

Anti-carrageenin paw edema effects of 1-(m-trifluoromethylphenyl)-3-(2-hydroxyethyl)-quinazoline-2, 4(1H, 3H)-dione [H-88] and 1-(m-trifluoromethylphenyl)-3-ethylpyridopyrimidine-2, 4(1H, 3H)-dione [HN-37] in rats were dissipated or reduced markedly by adrenalectomy. The effects of both compounds on the pituitary-adrenal axis were therefore investigated in male Wistar rats at 5-6 weeks of age. Oral treatments with H-88 in a dose of 100 mg/kg and HN-37 at 10 mg/kg induced the same degree of responses in intact animals, namely, a marked increase of blood corticosterone level at one hr of the peak time (360%), a decrease of adrenal ascorbic acid level at 3 hr (52-59%), an increase of blood glucose level at 6-12 hr (25-59%) and of liver glycogen level at 12-4 hr (97-153%). In addition, a significant hypertrophy of the pituitary and adrenals (p less than 0.05) at 6-12 hr and/or atrophy of the thymus and spleen at 3-24 hr were noted. The effect of HN-37 on blood corticosterone level was approximately 10 times as potent as that of H-88 as well as on the carrageenin paw edema. The effects of both compounds on blood corticosterone level were dissipated by adrenalectomy, and those on blood corticosterone level and adrenal ascorbic acid level were abolished by hypophysectomy. These results suggest that hypophysis-adrenal axis stimulation may play an important role in antiedematous effects of N-88 and HN-37.

Adrenal Glands↗

Effects of psychotropic drugs on pressor and behavioral responses to brain stimulation in unrestrained, unanesthetized rats.

Electrical stimulation of the posterior hypothalamus (PH) and the mesencephalic reticular formation (MRF) in unanesthetized, unrestrained rats with chronic electrode implants and an arterial cannula elicited a rise in blood pressure accompanied by behavioral changes such as exploration, flight or escape responses. Pentobarbital inhibited both the pressor and behavioral responses to PH and MRF stimulation. Chlorpormazine, diazepam and imipramine depressed the pressor response to PH stimulation rather than that to MRF stimulation with affecting the behavioral responses. It is concluded from these results that chlorpromazine, diazepam and imipramine exert their action on the neural pathway involved in the pressor response rather than on that inducing behavioral responses, whereas pentobarbital affects more extended brain areas related to these neural systems.

Animals↗