Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four effects of nomifensine were studied in interaction with a dopamine receptor blocker (pimozide) and a beta-adrenergic receptor blocker (propranolol). The effects of nomifensine were divided into two categories: 1. Psychomotor stimulant effect a) Stimulation of locomotor activity in mice b) Stereotyped behavior in rats 2. Antidepressant effect a) Antagonism of hypothermia caused by reserpine in mice b) Potentiation of yohimbine-induced toxicity in mice. The psychomotor stimulant effects were antagonized by pimozide but not by propranolol. The antidepressant effects were antagonized by propranolol but not by pimozide. Our results support the hypothesis that nomifensine acts via both dopaminergic and noradrenergic mechanisms subserving distinct behavioral effects, psychomotor stimulant and antidepressant, respectively.
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PMID:[Differences in the mechanisms of the stimulant and antidepressive effects of nomifensine]. 286 Feb 70

The effect of various doses of apomorphine (APO) (25, 250, 400 and 750 micrograms/kg, s.c.) on open field behaviour, stereotyped behaviour, body temperature and concentrations of serum oestradiol was studied in cycling females and in ovariectomized rats. With the exception of grooming, the hormonal variations during the cycle, or the ovariectomy, did not have an effect on behaviour related to stimulation of presynaptic dopamine (DA) receptors. The endocrine status on proestrus (PE), characterized by an increase in serum oestradiol, did influence hyperlocomotion and hypothermia induced by apomorphine; the former being attenuated and the latter increased, as compared to the other phases of the cycle. Ovariectomy resulted in an increase in the stimulatory effect of apomorphine on locomotion. Stereotypy induced by apomorphine was unaltered by hormonal variations during the cycle and it was slightly attenuated by removal of the ovaries. During phases of low levels of oestrogen (oestrus, metestrus) apomorphine significantly increased the levels of serum oestradiol, determined 30 min after the administration of drug. It is concluded that the various DAergic mechanisms in brain are differentially affected by hormonal variations during the cycle and by ovariectomy.
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PMID:Apomorphine-induced behaviour during the oestrous cycle of the rat. 365 16

The effects of various doses of estrogen on apomorphine (Apo)-induced hypothermia and stereotypy were investigated in ovariectomized rats. Daily administration of estradiol (5, 15 or 100 micrograms/kg) for 4 days or estradiol (100 micrograms/kg) for 3 days, followed by 4 and 72 hr withdrawal periods respectively, had no effect on apomorphine-induced hypothermia or stereotypy in a cold (4 degrees C) environment, although both effects were blocked by haloperidol. Large doses of estradiol (100 micrograms/kg) given for 3 days, followed by either 24 or 72 hr withdrawal, slightly attenuated apomorphine-induced stereotypy at 22 degrees C. Stereotypy observed at 22 degrees C was of greater magnitude than that seen at 4 degrees C. The results indicate that although high, non-physiological levels of estrogen may attenuate striatal-dependent stereotypies, this hormone has no detectable influence on dopaminergic mechanisms in the preoptic-anterior hypothalamic regions that are thought to mediate apomorphine-induced hypothermia.
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PMID:The effects of estrogen on apomorphine-induced hypothermia and stereotypy in the rat. 668 92

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

The administration of nafadotride, given at doses known to block the D3 dopamine receptors (0.75, 1.5, 3 mg/kg i.p.) increased locomotor activity both in naive and habituated rats and counteracted the hypothermia but not the hypomotility induced by a low dose of the putative D3 dopamine agonist (+/-)-7-hydroxy-2-(di-N-propylamino)-tetralin (7-OH-DPAT; 0.04 mg/kg). Nafadotride did not antagonize either the motor effects induced by different doses of the D2 agonist quinpirole (0.05 and 0.3 mg/kg) or the hypermotility induced by 7-OH-DPAT given at a dose (0.32 mg/kg) stimulating D2 dopamine receptors. The same nafadotride doses potentiated the grooming behavior induced by the D1 dopamine agonist SKF 38393 (10 mg/kg i.p.) as well as the stereotyped response to the D1/D2 agonist apomorphine (0.5 mg/kg s.c.). Stereotyped behavior was also observed in rats concomitantly treated with nafadotride and the D2 agonist quinpirole. As the activation of D1 dopamine receptors plays an important role in the occurrence of stereotypies, the results suggest that the blockade of D3 receptors by nafadotride could have favored D1/D2 dopamine receptor-mediated behaviors by potentiating D1 receptor function.
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PMID:Nafadotride administration increases D1 and D1/D2 dopamine receptor mediated behaviors. 1247 13