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C Kamei

Publications and source records attributed to C Kamei.

At least 127 records · Page 7Linked to original sources

Analgesic activity of certain tripeptide-beta-phenethylamide analogs.

Studies of the analgesic effect of tripeptide-beta-phenethylamides are described, and their structure-activity relationship is discussed. SD-25, which has a methyl group at R2, and a hydroxymethyl group at R3 of beta-phenethylamide, was the most potent one of the 8 analogs tested.

Analgesia↗

Epileptogenic activity of cephalosporins in rats and their structure-activity relationship.

The epileptogenic properties of 10 cephalosporins and penicillin G were compared by intraventricular application to rats. At doses greater than 32 micrograms per head, cefazolin provoked tremendous seizure signs, a spike-and-wave complex appeared in close succession for more than 30 min, and severe convulsions were observed repeatedly. Reactions to cefotiam, ceftezole, and cephaloridine were almost equal to reactions to penicillin. No epileptogenic signs were observed on EEGs, and no behavioral symptoms were observed after administration of 1,000 micrograms of cephalexin and cephradine per head. Reactions to cephapirin, cefmetazole, cephalothin, and ceftizoxime exhibited less marked epileptogenic features; activity was diminished in that order on EEGs and in behavioral signs. Compounds substituted with two different heterocyclic rings at position 7 (R1) and position 3 (R2) of 7-aminocephalosporanic acid were potent in producing epileptogenic signs both on EEGs and in behaviors. Compounds substituted with a heterocyclic ring at either position of 7-aminocephalosporanic acid were less potent. Compounds such as ceftizoxime, cephalexin, and cephradine, substituted at R2 with small groups, were almost incapable of producing epileptogenic activity. This may indicate that the substitution of a heterocyclic ring at position 3 will provoke the convulsive actions.

Animals↗

Effects of certain antiepileptics on cephaloridine- and cefazolin-induced seizures in rats.

Effects of phenobarbital, phenytoin and diazepam on cephaloridine-induced spiking activity (focal seizure) and cefazolin-induced violent seizure appearing repeatedly in EEG and general behavior (repeated generalized seizure) were studied in rats with chronically implanted electrodes. Phenobarbital, phenytoin and diazepam showed remarkable inhibition on cephaloridine-induced focal seizure and the ED50 values were 4.52 mg/kg, 9.41 mg/kg and 0.86 mg/kg, respectively. Phenobarbital and diazepam also inhibited cefazolin-induced repeated generalized seizure. The ED50s to inhibit seizure pattern in EEG were 30.5 mg/kg and 3.4 mg/kg, respectively and the ED50 values to suppress seizure behavior were 49.0 mg/kg and 4.7 mg/kg. However, phenytoin did not suppress repeated generalized seizure even at 100 mg/kg. From these results, cephaloridine-induced focal seizure and cefazolin-induced generalized seizure are thought to be useful models for evaluating the inhibitory effect of test compounds on cortical seizure and status epilepticus, respectively.

Animals↗

Effects of 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810) and some antiepileptics on the kindled seizures in the neocortex, hippocampus and amygdala in rats.

Effect of 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810) on kindled seizures in the neocortex, hippocampus and amygdala was studied in comparison with that of clinically proved antiepileptics, and the differences in kindled seizure development in the three areas were also studied. The amygdala more rapidly developed a generalized seizure (kindled seizure) than the hippocampus and the neocortex. Although more days of stimulation were needed, the neocortex also developed a kindled seizure similar to limbic kindled seizures. Phenobarbital, carbamazepine, dipropylacetate and diazepam showed a depressant effect on the neocortical kindled seizures. Phenytoin showed a depressant effect only when it was administered intravenously. Phenobarbital and carbamazepine depressed the hippocampal kindled seizures, while phenytoin and diazepam had little effect. Phenobarbital and diazepam caused marked depression on the amygdaloid kindled seizures, but the effect of phenytoin, carbamazepine and dipropylacetate on them was weak or negligible. AD-810 showed a depressant effect on neocortical and hippocampal kindled seizures, but not on amygdaloid ones. The profile of AD-810 is similar to that seen with carbamazepine.

Amygdala↗

Developmental change of EEG in rat from 4th to 16th week.

The development of EEG in 8 male rats from 4 to 16 weeks age were studied chronically. Theta band had the highest power at 5--16 weeks. Especially after 11 weeks, theta band presented a significantly higher peak than that of 4-week-old. In contrast to this, delta band, which had the highest power at 4 weeks, was markedly decreased.

Aging↗

Differential antagonism of antiavoidance, cataleptic and ptotic effects of neuroleptics by biperiden.

The interaction between neuroleptics and an anticholinergic, biperiden, in the antiavoidance, catalepsy and ptosis tests was investigated in mice for the purpose of predicting the extrapyramidal side-effects of neuroleptics. The cataleptic effect of most neuroleptics used was antagonized to some extent by biperiden, while the ptotic effect was hardly influenced. The antiavoidance effect of haloperidol, trifluperidol and perphenazine was markedly antagonized and that of chlorpromazine moderately. However, the effect of thioridazine, chlorprothixene, levomepromazine and clozapine was little antagonized. In neuropharmacological tests, haloperidol, trifluperidol and perphenazine exhibited a selective antidopaminergic activity, while chlorprothixene, levomepromazine and clozapine showed antidopaminergic, antiadrenergic and also anticholinergic activities when similar doses were given. These results indicate that biperiden antagonism may be marked in the tests related to the extrapyramidal symptoms and in drugs liable to induce extrapyramidal side effects, however, there would be little or no antagonism in drugs possessing the anticholinergic property and eliciting few extrapyramidal side-effects.

Animals↗

Effects of antiepileptics on both behavioral and electrographic seizure patterns induced by maximal electroshock in rats.

Effects of antiepileptics on both behavioral (TE) and electrographic seizure patterns induced by maximal electroshock were studied simultaneously in the same animal. The results obtained are as follows. All the antiepileptics used in this study depressed the TE seizure. Imipramine, biperiden, and lidocaine also depressed TE seizure, although they are not classified as antiepileptics. Phenobarbital, primidone, trimethadione, carbamazepine, ethosuximide, diazepam, clozapine, and imipramine had a depressant effect on electrographic seizures. However, phenytoin, ethotoin, phenacemide, and acetazolamide did not influence the electrographic seizure, in spite of having a strong effect on TE seizure. The present procedure, i.e., that of simultaneous observation of both behavioral and electrographic seizure patterns induced by maximal electroshock in the same animal, provides information which cannot be obtained from either behavior or EEG observation alone.

Animals↗

Effects of antidepressant drugs on amygdaloid after-discharge in rats.

Effects of antidepressant drugs on the amygdaloid after-discharge induced by stimulating the amygdala in rats implanted with chronic electrodes, were investigated in correlation with anti-muricidal effects as well as neurotoxicity. Tricyclic antidepressants such as amitriptyline, imipramine and nortriptyline markedly depressed both after-discharge and muricide at doses smaller than neurotoxic doses. The effect of PF-257 was also the same as tricyclic antidepressants. On the other hand, methamphetamine and pipradrol blocked the muricide at doses smaller than neurotoxic doses without depressing the amygdaloid after-discharge. Major tranquilizers, chlorpromazine and clozapine depressed both after-discharge and muricide only at doses larger than those which impaired rotarod performance. Haloperidol, on the contrary, depressed the after-discharge without selectively blocking the muricide. Minor tranquilizers, diazepam and chlordiazepoxide did not block the muricide at doses smaller than neurotoxic doses, although they showed a marked depression of the after-discharge.

Amitriptyline↗

Effects of anti-Parkinsonian drugs on neurobehavioural changes induced by bilateral 6-hydroxydopamine lesions in rats.

1. Effects of anti-Parkinsonian drugs on neurobehavioural changes induced by bilateral lesions of dopaminergic neurons were investigated in rats. 2. Dopaminergic neurons in rats were lesioned bilaterally by injection of 6-hydroxydopamine (6-OHDA; 8 micrograms) into the medial forebrain bundle at the level of the posterolateral hypothalamus. As a result, a decrease in locomotor activity and marked catalepsy and prolongation of grasping time were observed. 3. Levodopa, talipexole, bromocriptine and theophylline dose-dependently antagonized the decrease in locomotor activity induced by bilateral 6-OHDA lesions. These drugs also showed antagonistic effects on the appearance of catalepsy and prolongation of grasping time induced by bilateral 6-OHDA lesions. In contrast, trihexyphenidyl showed no antagonizing effect on the neurobehavioural changes induced by 6-OHDA lesions at any concentration tested. 4. Combined treatment with levodopa and talipexole antagonized the neurobehavioural changes induced by bilateral 6-OHDA lesions, whereas no marked changes were observed when either drug was administered separately. The same findings were noted with the simultaneous use of either levodopa (2 mg/kg) and theophylline (2 mg/kg) or talipexole (0.005 mg/kg) and theophylline (2 mg/kg). 5. These results indicate that this model may be useful for estimating the effects of drugs in the treatment of Parkinson's disease.

Animals↗

Effects of antiallergic drugs on histamine release from rat peritoneal mast cells induced by bradykinin.

Effects of antiallergic drugs on bradykinin-induced histamine release and intracellular Ca2+ release from peritoneal mast cells were studied in rats. Bradykinin caused a concentration-dependent histamine release as well as Ca2+ release from the intracellular Ca store of peritoneal mast cells. Antiallergic drugs used in this study showed an inhibition of not only histamine release but also Ca2+ release. The Ca2+ release from the intracellular Ca store induced by bradykinin was more sensitive to antiallergic drugs than histamine release from mast cells. Mequitazine and terfenadine caused potent inhibitory effects on both responses, whereas effects of ketotifen and cromolyn sodium were relatively weak. In conclusion, histamine release from mast cells and intracellular C2+ release induced by bradykinin were inhibited by antiallergic drugs similar to those induced by substance P and compound 48/80.

Animals↗