Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examined the behavioral, neurochemical and endocrinological characteristics of aggressive, male alpha-mice. These mice inflict severe bite marks on other male mice in their cage, but are not attacked themselves. The characteristics of the alpha-mice were compared with those of submissive mice, and of control mice taken from cages in which no severe fighting was observed. The behavioral tests used were Porsolt's swim test of behavioral 'despair', a plusmaze test of anxiety, a holeboard test of exploration and locomotor activity, and a test of seizure threshold to bicuculline. The alpha-mice were found to be immobile in the swim test for a shorter time than the submissive and control mice, and the submissive mice for a longer time than the controls. In the holeboard, the alpha-mice spent less time making exploratory head-dips than the other mice. Submissive mice had elevated 5-HIAA levels in the hypothalamus, hippocampus and brainstem, and the alpha mice had reduced concentrations of dopamine in the brainstem. There were no significant differences in plasma corticosterone or testosterone concentrations between the groups. These findings indicate that in alpha-mice, a number of behavioral and neurochemical characteristics appear together with the unusually high aggressiveness towards cage-mates.
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PMID:Behavioral, hormonal and neurochemical characteristics of aggressive alpha-mice. 281 52

When epileptic seizures occur suddenly in puberty, the patient is seized with the feeling of anxiety, isolation and despair, and this feeling is increased by the special quality of puberty. The patient tries to overcome this critical situation by including "epilepsy" in his own personality. When this process is accomplished in puberty in which an ego-identification is done, an epileptic personality disorder is formed gradually. Accordingly, how the patient tides over this crisis is important for the formation of an epileptic personality disorder. In order to prevent the development of this condition, it is necessary to apply psychotherapy.
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PMID:[Reflections on epileptic personality changes]. 746 8

The effect of the 5-HT1A agonist SR 57746A (1-[2-(naphth-2-yl) ethyl]-4-(3-trifluoromethylphenyl))-1,2,5,6 tetrahydropyridine hydrochloride), was evaluated in a variety of psychopharmacological tests in rodents. In the approach-avoidance conflict test in rats, orally administered SR 57746A significantly increased punished responding at doses as low as 3 mg/kg, while unpunished responding was only reduced at 30 mg/kg. SR 57746A was active for at least 4 hours in this test. SR 57746A significantly antagonised the lithium-induced taste aversion in rats at doses of 3 and 10 mg/kg po. In staircase test in mice, SR 57746A reduced rearing at doses which did not reduce the number of steps climbed. In the two-compartment exploratory model in mice, SR 57746A increased the latency to the first entry into the dark compartment (at 2 to 8 mg/kg po), and reduced the time spent in the dark compartment (at 8 mg/kg po), but had no effect on the total number of transitions. SR 57746A potently reduced aggressive behaviour in isolated mice, the dose of 1 mg/kg po produced over 80% inhibition of fighting in this test. SR 57746A was also active in the behavioural despair test of depression in mice and rats, and reversed learned helpless behaviour in rats. SR 57746A was also active in the behavioural despair test of depression in mice and rats, and reversed learned helpless behaviour in rats. SR 57746A dose-dependently generalised to the cue produced by 8-OH-DPAT in rats, but produced only a very weak serotonergic syndrome. Like 8-OH-DPAT and ipsapirone, SR 57746A reduced body temperature in mice, but only at a high dose (10 mg/kg po). SR 57746A reversed haloperidol-induced catalepsy in rats with an ED50 of 3.85 mg/kg po, but was unable to antagonise the stereotypy induced by apomorphine in this species. SR 57746A was inactive or only very weakly active in a series of tests typical of benzodiazepine-like activity, including antagonism of pentetrazol-induced seizures, reduction of muscle tone and locomotor activity, impairment of motor co-ordination, and potentiation of the effects of centrally-acting sedative-hypnotics. SR 57746A was also inactive as an analgesic in the PBQ writhing test. Thus, SR 57746A is active in a number of tests indicative of 5-HT1A receptor stimulation in vivo, and, more particularly, in a number of tests predictive of anxiolytic, anti-aggressive and antidepressant activities. SR 57746A is as potent as diazepam in anxiolytic tests, and more potent than imipramine in antidepressant tests, whereas it is devoid of neuroleptic potential. In view of this profile of activity, SR 57746A merits evaluation as a potential anxiolytic and antidepressant in humans.
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PMID:Neuropsychopharmacological profile in rodents of SR 57746A, a new, potent 5-HT1A receptor agonist. 790 76

The neuropharmacological profile of the total fungal extract of F. moniliforme (FM) has been investigated. FM produced dose related decrease in spontaneous motor activity (SMA) and exploratory activity, potentiated pentobarbitone hypnosis and the anticonvulsant actions of phenobarbitone and phenytoin against MES seizures, potentiated PTZ and tryptamine seizures, antagonised reserpine induced syndrome, attenuated tetrabenazine and morphine induced catalepsy and potentiated haloperidol catalepsy. FM showed per se antinociceptive activity and potentiated morphine analgesia. It increased rectal temperature, antagonised reserpine and apomorphine hypothermia and potentiated the hyperthermic response of haloperidol and 5-hydroxytryptophan (5-HTP) and hypothermic response of betaphenylethylamine (PEA) and L-dopa. FM had no per se effect on amphetamine lethality, but enhanced the lethality induced by morphine in aggregated animals. Stereotypy by amphetamine was potentiated while that of apomorphine was not affected. The behavioural response of 5-HTP and L-dopa was potentiated. FM had no effect on swim induced behavioural despair. The effect on aggressive behavior was complex, and while the cumulative aggressive score was reduced, the onset of fighting behaviour and contact period was increased. It also inhibited clonidine induced auto mutilation. Since earlier investigation had shown that FM, like nialamide, induced non-selective inhibition of monoamine oxidase (MAO), the results were compared with those induced by nialamide. A comparative profile of action reveals that the neuropharmacological action of FM are qualitatively similar to those induced by nialamide, and likely to be due to inhibition of MAO. The investigation has practical implications because F. moniliforme is a common contaminant of cereals and fruits.
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PMID:Neuropharmacological studies on Fusarium toxins--I: Total toxin extract from Fusarium moniliforme. 906 73

We present a case of reflex-induced simple partial seizures, triggered by feelings of frustration, anger and despair. Such emotions were provoked by pondering over complex national and international, political and moral issues. The present case may suggest that activation of right temporal networks may mediate negative and adverse emotions induced by preoccupation with agitating, controversial issues.
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PMID:Seizures induced by frustration and despair due to unresolved moral and political issues: a rare case of reflex epilepsy. 1006 77

The effect of nitrendipine (NTP) alone and in combination with phenytoin (PHT) and valproate (VPA) against maximal electroshock seizures (MES) was studied in rats. In addition, the psychomotor effects of NTP alone and in combination with PHT and VPA were evaluated using the following tests: a) rotarod performance; b) spontaneous motor activity; c) despair behavior; d) righting reflex; e) hole board test; and f) passive avoidance test. ED50 values of PHT, VPA and NTP were 13,255 and 3.6 mg/kg, respectively. When NTP was combined with PHT or VPA, the ED50 values decreased to 0.9 and 226 mg/kg, respectively. In the psychomotor function tests, for the same degree of protection (50%) afforded against MES, PHT or VPA produced a greater impairment in all the parameters compared to NTP alone or a combination of NTP with PHT or VPA. Furthermore, NTP reversed the depression and long-term memory loss induced by PHT and VPA. Thus, NTP was effective against MES in rats, potentiating the anti-electroshock activity of PHT and VPA and producing less impairment of psychomotor activity. Thus, the agent can be considered a potential antiepileptic warranting further studies.
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PMID:Anticonvulsant and psychomotor activity of nitrendipine alone and in combination with phenytoin and valproate in rats. 1044 38

The present study evaluated the effects of mixed opioid drugs on the severity of cocaine (COCA) toxicity by examining stress-related behavioral alterations in mice. In order to ascertain the strength of the stress, the continuous observation of the behavioral symptoms in the cage and the forced swimming test (Porsolt test) were performed in the COCA (75 mg/kg, i.p.)-treated groups, with or without the mixed mu-kappa receptor-related opioid drugs, buprenorphine (BUP) and pentazocine (PEN). Using the high-sensitivity activity measuring instrument Supermex, both the spontaneous behaviors in the cage and the forced swimming behaviors in the water were assessed as activity counts. The behavioral alterations in the COCA-treated groups were compared with a group of mice given a 10 min immobilization stress (IM group). In the COCA-only group, a prolonged increase in the spontaneous behaviors accompanied by convulsive seizures was observed even in the surviving mice, unlike in the IM group. However, an acceleration of behavioral despair in the Porsolt test similar to that observed in the IM group was observed in the COCA group after the disappearance of the acute toxic symptoms (5 hours after the COCA treatment). Among the opioid-treated groups, the mortality rate was attenuated only in the COCA-BUP (0.25 mg/kg, i.p.) group. In the COCA-BUP group, a prolonged suppression of the morbid hyperactivity in the cage except for the convulsive seizures, and a normalization of the swimming behavior in the Porsolt test were observed in the survivors. On the other hand, in the COCA-PEN (5 mg/kg, i.p.) group, the swimming behavior in the Porsolt test was abnormally increased in addition to the prolonged morbid hyperactivity in the cage. Therefore, the COCA-induced stress-related behaviors were normalized in the group of mice treated with BUP, a group with a good prognosis.
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PMID:Stress-related behavioral alterations accompanying cocaine toxicity: the effects of mixed opioid drugs. 1119 74

The effect of nimodipine alone and in combination with diazepam or phenytoin was tested in the electroshock-induced mouse model of status epilepticus. Status epilepticus was induced by transauricular electrical stimulation with a stimulus of 15 mA at 0.5, 3, 10, 20 and 30 min, starting half an hour after intraperitoneal administration of vehicle/drug. The median effective doses of diazepam and phenytoin alone and in combination with a fixed dose of nimodipine (24 mg/kg) was calculated. The ED50s of diazepam and phenytoin were found to be 10.5 and 9 mg/kg, respectively. When nimodipine was combined with diazepam or phenytoin, the ED50 values decreased to 3.77 mg/kg and 7.15 mg/kg, respectively. The severity of seizures was also decreased by combination with nimodipine as compared to diazepam and phenytoin given alone. To study the effect of nimodipine on psychomotor impairments produced by diazepam and phenytoin three tests were performed: rotarod, behavioral despair and hole board. Nimodipine did not show protective effects on its own but potentiated the anticonvulsant effects of diazepam and phenytoin. Furthermore, the combination of nimodipine with diazepam and phenytoin produced lesser impairment of psychomotor functions.
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PMID:Anticonvulsant effect of nimodipine alone and in combination with diazepam and phenytoin in a mouse model of status epilepticus. 1134 93

The phenyl (thio) semicarbazide derivatives of phthalimido pharmacophore were synthesized and evaluated for their anticonvulsant and neurotoxic properties. Initial anticonvulsant screening was performed using intraperitoneal (i.p.), maximal electroshock-induced seizure (MES), subcutaneous pentylenetetrazole (scPTZ) and subcutaneous strychnine (sc STY)-induced seizure threshold tests in mice. Compound 2c afforded protection in all the three screens. Compounds except 1d, 2a and 2d showed no neurotoxicity up to 300 mg/kg. Compounds 1a, 1b, 2c, 2d, 2g and 2i were found to show oral MES activity. The compounds exhibited CNS depression and behavioral despair side effects, lesser than the conventional antiepileptic drugs.
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PMID:Synthesis and anticonvulsant and neurotoxicity evaluation of N4-phthalimido phenyl (thio) semicarbazides. 1459

Twelve 1-phenyl-, 1-thiocarbamoyl- and 1-N-substituted thiocarbamoyl-3-(2-furyl)-5-phenyl/(2-furyl)-2-pyrazoline derivatives were synthesized. The chemical structures of the compounds were proved by IR, (1)H NMR, Mass spectrometric data and microanalyses. The antidepressant activities of the compounds were investigated by Porsolt's behavioural despair (forced swimming) test on albino mice. 1-N-Ethylthiocarbamoyl-3-(2-furyl)-5-phenyl-2-pyrazoline (6) and 1-N-allylthiocarbamoyl-3,5-di(2-furyl)-2-pyrazoline (11) reduced 33.80-31.42% duration of immobility times at 10 mg kg(-1) dose level. Anticonvulsant activities of the compounds were determined by maximal electroshock seizure (MES) and subcutaneous pentylenetetrazole (metrazol) (scMet.) tests, neurotoxicities were determined by rotarod toxicity test on albino mice. 1,5-Diphenyl-3-(2-furyl)-2-pyrazoline (2), 1-N-allylthiocarbamoyl-3-(2-furyl)-5-phenyl-2-pyrazoline (7), 1-N-allylthiocarbamoyl-3,5-di(2-furyl)-2-pyrazoline (11) and 1-N-phenylthiocarbamoyl-3,5-di(2-furyl)-2-pyrazoline (12) were active at 100-300 mg kg(-1) dose levels. 1-Thiocarbamoyl-3,5-di(2-furyl)-2-pyrazoline (4), 1-N-methylthiocarbamoyl-3,5-di(2-furyl)-2-pyrazoline (9) and 1-N-ethylthiocarbamoyl-3,5-di(2-furyl)-2-pyrazoline (10) were found protective against MES and scMet. at 30-300 mg kg(-1) dose levels.
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PMID:Synthesis and studies on antidepressant and anticonvulsant activities of some 3-(2-furyl)-pyrazoline derivatives. 1706 33


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