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Biomedical subjects

S Ueki

Publications and source records attributed to S Ueki.

At least 235 records · Page 13Linked to original sources
PubMed1977

Characteristics in aggressive behavior induced by midbrain raphe lesions in rats.

Midbrain raphe lesions induced aggressive behavior which was characterized by defensive aggression rather than offensive aggression in nature. Furthermore, raphe-lesioned rats exhibited muricide. This muricide included not only mouse-killing but also mouse-eating behavior. Both dorsal and medial raphe lesioned (dm-R) rats exhibited much greater hyperemotionality than either the dorsal (d-R) or medial raphe lesioned (m-R) rats, though no significant difference was found between d-R and m-R rats. It is concluded that the characteristic of aggression induced by raphe lesions is different in many respects from that induced by p-chlorophenylalanine administration, olfactory bulbectomy and septal lesions.

Aggression↗
PubMed1977

Biochemical correlates in mouse-killing behavior of the rat: prolonged isolation and brain cholinergic function.

After 30 days of isolation, 45% of the rats exhibited mouse-killing behavior. The killing response was suppressed by atropine (5 mg/kg and 8 mg/kg, IP) and scopolamine (8 mg/kg, IP), whereas methylatropine was ineffective. Acetylcholine (ACh) content and acetylcholinesterase (AChE) activity were measured in 5 discrete areas of rat brain. As compared with the aggregated rats only the killer rats exhibited higher ACh levels in the diencephalon. The activity of AChE in all brain areas was unchanged by isolation; no significant difference was found between the killer and nonkiller rats. These results suggest that central cholinergic mechanisms participate in the mediation of mouse-killing behavior in the rat.

Acetylcholine↗
PubMed1977

[Behavioral effects of 5-(o-chlorophenyl)-1-methyl-7-nitro-1,3-dihydro-2H-1,4-benzodiazepin-2-one (ID-690)].

Effects on the central nervous system of ID-690, a new benzodiazepine derivative were investigated and compared mainly with those of diazepam in mice and rats. Locomotor activity of the rat was increased with ID-690, at doses of 2 approximately 5 mg/kg p.o., as with diazepam. ID-690 was approximately 5 times more potent than diazepam in inhibiting fighting behavior of long-term isolated mice. Hyperemotionality induced by either septal lesions or olfactory bulbectomy was also inhibited by ID-690. This effect was almost the same in potency as that of diazepam. ID-690 was only 1/30 as potent as diazepam in preventing maximal electroshock convulsion, while it was approximately 18 times more potent that diazepam in suppressing pentetrazol convulsion in mice. ID-690 was approximately 5 times as potent as diazepam in impairing rotarod performance in mice. The muscle relaxant effect of ID-690 was approximately 10 times as potent as diazepam, as measured with an inclined screen test in mice. Thus the effect of ID-690, as compared with diazepam, was characterized by its relatively potent muscle relaxant and extremely potent anti-pentetrazol convulsant action.

Agonistic Behavior↗
PubMed1977

[Electroencephalographic effects of chlorphenesin carbamate, a new central muscle relaxant, in rabbits (author's transl)].

Electroencephalographic (EEG) effects of chlorphenesin carbamate were investigated in rabbits with chronic electrode implants, and compared with those of chlormezanone and methocarbamol. Chlorphenesin carbamate (50 mg/kg i.v., 100 mg/kg i.d.) induced a drowsy pattern of spontaneous EEG consisting of high voltage slow waves in the cortex and amygdala, and desynchronization of hippocampal theta waves. Chlormezanone also elicited similar EEG changes but such were much more potent than chlorphenesin carbamate. Methocarbamol showed no effect on spontaneous EEG. Chlorphenesin carbamate caused sedation in this period and muscle relaxation was more potent than that of chlormezanone. The EEG arousal response to auditory stimulation and to electric stimulation of the posterior hypothalamus, centromedian thalamus and mesencephalic reticular formation was slightly depressed by chlorphenesin carbamate. Chlorphenesin carbamate, as with chlormezanone, markedly depressed the limbic afterdischarges elicited by hippocampal stimulation. These EEG effects of chlorphenesin carbamate were qualitatively similar to but much weaker than those of chlormezanone, whereas the muscle relaxant effect of chlorphenesin carbamate was more potent than that of chlormezanone.

Acoustic Stimulation↗
PubMed1977

Possible involvement of a central noradrenergic system in automutilation induced by clonidine in mice.

Automutilation induced by a single large dose of clonidine was potentiated by pretreatment with methamphetamine, caffeine and theophyline, while it was inhibited by acute administration of reserpine, alpha-methyl-p-tyrosine, phenoxybenzamine, phentolamine and chlorpromazine. L-Dopa, 5-hydroxytryptophan and p-chlorophenylalanine had no effect on this abnormal behavior. Biochemical studies on brain monoamines revealed that noradrenaline was markedly increased and dopamine slightly so, but 5-hydroxytryptamine was never changed by clonidine. These results suggest that a central noradrenergic system may be involved in automutilation induced by clonidine in mice.

5-Hydroxytryptophan↗
PubMed1977

Changes in sensitivity of mice to anticonvulsant drugs following bilateral olfactory bulb ablations.

Changes in sensitivity to anticonvulsant drugs were investigated after bilateral olfactory bulb ablations in mice. The sensitivity to benzodiazepines and acetazolamide increased, whereas that to phenylacetylurea and dipropylacetic acid decreased, and sensitivity to phenobarbital, diphenylhydantoin and trimethadion was not significantly changes after olfactory bulb ablations. Increase in sensitivity to benzodiazepines was the most significant in both electroshock and pentetrazol convulsions. It was suggested that altered activities and denervation supersensitivity in the limbic system, hypothalamus and midbrain might account for these changes in sensitivity to anticonvulsant drugs after olfactory bulb ablations.

Acetazolamide↗
PubMed1977

Cardiovascular changes induced by large doses of clonidine in mice.

Clonidine at doses of 0.5-1.0 mg/kg i.p. produced an initial rise followed by a sustained fall in blood pressure. The initial pressor response became more marked and the onset of hypotensive effect was delayed as the dose was increased to large doses such as 10-50 mg/kg given intraperitoneally. The heart rate was markedly reduced soon after clonidine administration and the bradycardia lasted for more than 2 hours. Both the initial pressor and subsequent hypotensive effects of clonidine were reduced by pretreatment with phentolamine, the initial pressor effects were suppressed by propranolol which did not affect the hypotensive effects. This initial pressor effect was potentiated while the hypotensive effect was reduced after bilateral vagotomy and pretreatment with either 6-hydroxydopamine or atropine. The bradycardia was significantly reduced by propranolol, atropine and bilateral vagotomy. Central sympathetic as well as parasympathetic mechanisms may be involved in cardiovascular changes after large doses of clonidine in urethanized mice.

Animals↗
PubMed1976

[Electroencephalographic effects of lopramine].

Electroencephalographic (EEG) effects of lopramine, a new antidepressant, were investigated in rabbits with chronic electrode implants, and compared with those of imipramine and amitriptyline. All drugs were administered i.v. Lopramine (10, 20 mg/kg) induced a drowsy pattern of spontaneous EEG consisted of high voltage slow waves in the cortex and amygdala, and desynchronization of hippocampal thetha waves. Imipramine and amitriptyline (1-5 mg/kg) also elicited similar EEG changes but were much more potent than lopramine in this effect. Lopramine (10, 20 mg/kg) failed to suppress the EEG arousal responses induced by not only auditory stimulation but also electrical stimulation of the mesencephalic reticular formation, centromedian thalamus and posterior hypothalamus, whereas imipramine and amitriptyline (1 approximately 5 mg/kg) markedly inhibited these responses. The EEG arousal response induced by i.v. injection of physostigmine 0.1 mg/kg showed no change after lopramine (20 mg/kg), while the response was significantly suppressed by imipramine (2, 5 mg/kg) and amitriptyline (1, 2 mg/kg). Lopramine showed no effect on the recruiting response induced by electrical stimulation (8 Hz) of the centromedian thalamus and slightly enhanced the limbic afterdischarges elicited by either hippocampal or amygdaloid stimulation, while imipramine (2, 5 mg/kg) and amitriptyline (1--5 mg/kg) caused an initial depression followed by sustained enhancement of these afterdischarges. These results demonstrate lopramine to be an antidepressant of a new type which has no effect on the ascending reticular activating system and no central anticholinergic action.

Amitriptyline↗
PubMed1976

[Behavioral pharmacology of a new antidepressant, lopramine].

The behavioral effects of lopramine [N-methyl-N-(4-chlorobenzoyl-methyl)-3-(10, 11-dihydro-5H-dibenz (b,f) azepin-5-yl) propylamine hydrochloride] were investigated in mice and rats and compared with those of amitriptyline and imipramine. Lopramine inhibited reserpine hypothermia and haloperidol catalepsy in mice and tetrabenazine ptosis in rats. In addition the drug potentiated the effects of methamphetamine, and DOPA- or apomorphine-induced stereotypy in mice, whereas it suppressed muricide of the rat induced by either olfactory bulbectomy or delta9-tetrahydrocannabinol, similar to the responses seen with imipramine and amitriptyline. On the other hand,lopramine increased spontaneous motor activity and markedly potentiated methamphetamine hyperactivity. In contrast to imipramine and amitriptyline, lopramine failed to counteract both the lethal effect of physostigmine and oxotremorine tremor in mice, indicating that the drug had no central anticholinergic effect. Lopramine, even at such a large dose as 5,000 mg/kg p.o., caused neitherimpairment of coordinated motor activity nor muscle relaxation. It is concluded that lopramine is a new type of tricyclic antidepressant with extremely low toxicity and without central anticholinergic action.

Amitriptyline↗
PubMed1975

Automutilation induced by clonidine in mice.

Clonidine (2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride, St155, Catapres), after administration of a single large dose, was found to induce automutilation in mice housed individually in the absence of objects to bite. This abnormal behavior was not significantly altered with chronic administration of the drug, and showed no behavior induced by the same drug in mice caged in groups.

Animals↗