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)

Imidazole (IMID) inhibited (+/-) N-n-propylnorapomorphine (NPA) and BHT-920 induced penile erections (PE) and stretching and yawning (SY) in rats as well as apomorphine (APO) induced hypothermia in mice, enhanced shock-elicited aggressiveness in rats and antagonized sleep induced by clonidine in chicks. IMID moreover displayed activity in behavioural tests used in specific screening for antidepressants, potentiating yohimbine toxicity in mice and antagonizing immobility time in the despair test, with a potency in some cases equal to imipramine. IMID per se, depressed motor activity in both mice and rats. The possible mechanism of action and receptors involved are briefly discussed as well as IMID's profile as an antidepressant drug.
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PMID:Behavioural pharmacology of imidazole, a potential antidepressant agent. 406 41

Antihistaminics of various chemical structures: chlorcyclizine, chloropyramine, chlorpheniramine, clemastine, diphenhydramine, mepyramine, promethazine, and thenalidine were investigated for the action in tests for antidepressant drugs. The antihistaminics did not affect significantly the spontaneous locomotor activity of rats. Most of them (chloropyramine, chlorpheniramine, diphenhydramine, promethazine and thenalidine) increased amphetamine hypermotility but chlorcyclizine significantly inhibited, and clemastine and mepyramine did not affect it. In mice, chlorcyclizine, mepyramine and promethazine inhibited amphetamine hypermotility, while others antihistaminics were without effect. L-DOPA-induced hypermotility in mice was inhibited by all compounds tested. With the exception of chlorpheniramine and mepyramine, all tested antihistaminics produced hypothermia in mice, although fife of them (chlorpheniramine, diphenhydramine, chlorcyclizine, chloropyramine and thenalidine) antagonized the reserpine-induced hypothermia. With the exception of mepyramine and clemastine, the compounds tested shortened the period of immobility of rats in the behavioral despair test. The results indicate that only few antihistaminics have pharmacological profile resembling tricyclic or atypical antidepressant drugs.
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PMID:Effects of antihistaminic drugs in tests for antidepressant action. 611 82

The atypical neuroleptic sulpiride is also prescribed for depression because of its activating effect. However, such an effect does not necessarily imply an action identical to that of classical antidepressants, and a laboratory comparison of the neuroleptic and antidepressant activities of sulpiride may contribute to a better definition of its psychotherapeutic profile. Sulpiride isomers were studied in the rat in four behavioural models of depression which are thought to be influenced by neuroleptics in different ways. Desipramine (imipramine) and haloperidol were employed in each test as a standard antidepressant and neuroleptic, respectively. The four tests were: 1) prevention of apomorphine-induced sedation: 2) antagonism of apomorphine-induced hypothermia; 3) behavioural despair (swim test); 4) learned helplessness ( FR2 lever pressing escape). Desipramine ameliorated behaviour in all tests; haloperidol ameliorated the response to test 1, influenced that to test 2 in a neuroleptic-like way and worsened the responses to tests 3 and 4. (-)-Sulpiride worked in a similar way to haloperidol in all tests. (+)-Sulpiride significantly and dose-dependently ameliorated the responses to test 3 and was inactive in the others. No conclusion was drawn from test 1 owing to its lack of specificity; the results of the remaining tests indicated a neuroleptic profile of (-)-sulpiride and suggested a potential "antidepressant" activity of (+)-sulpiride which merits further investigation.
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PMID:Antidepressant versus neuroleptic activities of sulpiride isomers on four animal models of depression. 614 54

Effects of three phosphodiesterase (PDE) inhibitors (rolipram, IBMX, and Ro 20-1724) were studied in mice in some tests predictive for antidepressant activity. All the drugs antagonized reserpine-induced hypothermia and slightly antagonized reserpine-evoked hypoactivity. Rolipram and IBMX were also effective in behavioral despair test. On the other hand, the examined PDE inhibitors did not affect apomorphine-induced hypothermia and did not potentiate the central action of L-DOPA. These results show that psychopharmacological profile of the PDE inhibitors differs from that of classical imipramine-like antidepressants.
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PMID:Antidepressant properties of some phosphodiesterase inhibitors. 619 18

This research compares the effects, in mice and rats, of desmethylclomipramine (DCLOM) and clomipramine (CLOM). DCLOM antagonized the hypothermia induced in mice by reserpine or apomorphine to a much greater extent than CLOM. Reserpine ptosis in mice was depressed by DCLOM only. Similarly, only DCLOM was effective in the behavioral despair test in rats. DCLOM increased the 5-hydroxytryptamine (5-HT) pressor effect in pithed rats, but to a lesser extent than CLOM by several factors. Only DCLOM increased the noradrenaline (NA) pressor effect. The depletion of NA induced by 6-hydroxydopamine was depressed by DCLOM only. The 5-HT depletion induced by p-chloromethamphetamine was antagonized only by CLOM. The results obtained show that the noradrenergic mechanism is of prime importance in the action of DCLOM and of much more importance than in the action of CLOM.
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PMID:Comparison of the pharmacological actions of desmethylclomipramine and clomipramine. 621 80

The pharmacological profile of salbutamol, an agonist of beta-adrenergic receptors and a potential antidepressant drug, and its effect on the central serotonin system were studied. It was found that salbutamol either had no effect, or, at higher doses, inhibited the spontaneous activity of mice and rats; it did not influence significantly either the produced by amphetamine locomotor stimulation (in mice and rats) or amphetamine stereotype (in rats). Salbutamol while not affecting body temperature of normal mice reversed hypothermia but not ptosis induced by reserpine, and counteracted the hypothermic action of apomorphine in mice. It neither affected the spiperone-induced catalepsy nor was active in the behavioural despair test in rats. Salbutamol had no effect either, on the fenfluramine-induced hyperthermia in rabbits, on the 5-hydroxytryptophan-induced head twitch reaction in mice, on the tryptamine-induced clonic convulsions of forepaw in rats on the flexor reflex in spinal rats, or on the quipazine- or fenfluramine-induced stimulation of this reflex. The above findings indicate that the pharmacological profile of salbutamol resembles that of classical imipramine-like antidepressant drugs to a very small extent and it does not affect the central serotonergic transmission.
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PMID:The central action of salbutamol, a beta-agonist with a potential antidepressant activity. 626 86

Minaprine (3-[2-morpholino-ethlamino]-4-methyl-6-phenyl-pyridazine dihydrochloride; 30038CM; trade name in France: Cantor) is a new psychotropic drug. The therapeutic profile of minaprine differs from that of other known psychotropic agents; in man the drug antagonizes the "inhibitory syndrome" characterized by decreased spontaneous activity, reduction in basic drives, slowed thoughts, feelings of tiredness and social withdrawal. Preliminary clinical trials have indicated that minaprine may also be effective in certain depressive states. This finding prompted us to study the effects of minaprine in animal models for depression. Like most antidepressants minaprine antagonizes behavioral despair, but the effect exhibits a slow onset and maximal activity is reached 24 h after administration. Minaprine also antagonizes reserpine-induced ptosis, this effect has a rapid onset, and is long-lasting. In contrast, minaprine poorly antagonizes reserpine-induced hypothermia. Unlike most antidepressants minaprine does not potentiate yohimbine-induced lethality. Minaprine potently antagonizes prochlorperazine-induced catalepsy in rats and potentiates amphetamine-induced stereotyped behavior, suggesting that the drug may enhance dopaminergic transmission. Finally, minaprine does not antagonize either oxotremorine-induced tremors or physiostigmine-induced lethality. Taken together the results of the present study indicate that minaprine is active on certain, but not all, animal models for depression and suggest the drug may have a potential clinical utility in the treatment of human depressions.
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PMID:Pharmacological evaluation of minaprine dihydrochloride, a new psychotropic drug. 689 Mar 59

Pirenzepine, (5,11-dihydro-11-[(4-methylpiperazin-1-yl)-acetyl]-6H-pyrido-[2,3] [1,4]-benzodiazepin-6-one dihydrochloride), tested on rats and mice, did not demonstrate any conspicuous behavioral action: it did not counteract reserpine hypothermia in mice, the L-DOPA hypermotility of mice, and (with the exception of very large doses) the amphetamine hypermotility in mice and rats. The drug neither prolonged the time of immobility of rats in the behavioral despair test, nor affected the central serotonin system in rats in tests for 5-hydroxytryptophan-induced head twitches, tryptamine-induced convulsions and fenfluramine-induced hyperthermia at high ambient temperature. Pirenzepine did not affect either the hind limb flexor reflex in the spinal rat, nor the action of serotoninomimetics of it. The investigated compound had strong peripheral cholinolytic action as it inhibited salivation and lacrimation in the oxotremorine test. The oxotremorine tremor was weakened only by very high doses of pirenzepine. LD50 of the drug in mice was 412 mg/kg ip.
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PMID:Central action of pirenzepine. 689 18

Proadifen (SKF 524 A) inhibited the following effects of imipramine (IMI), without affecting those of desipramine (DMI) in mice: antagonism towards reserpine-induced hypothermia, ptosis and sedation, antagonism to apomorphine hypothermia and insignificant shortening of the immobility time in the behavioral despair test. Cerebral levels of DMI were very low after administration of IMI; pretreatment with proadifen did not affect the already low levels of DMI but significantly elevated these of IMI. This may indicate that some other than DMI metabolites (e.g., 2-hydroxy-derivatives) may be of importance for the action of IMI in mice in the tests employed in this study.
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PMID:The effect of proadifen, a drug metabolism inhibitor, on action of imipramine and desipramine in mice. 718 47

A psychopharmacological profile of mesterolone, an androgen and potential antidepressant drug, was tested in mice and rats. Given in a dose of 80 mg/kg ip, mesterolone potentiated the action of L-DOPA in mice and in doses 40 and 80 mg/kg ip potentiated the amphetamine stereotypy in rats. On the other hand, in doses of 20--80 mg/kg ip mesterolone did not affect the reserpine induced hypothermia and ptosis, did not antagonize the apomorphine induced hypothermia in mice, did not change the motor stimulation produced by amphetamine and did not affect the spiperone induced catalepsy in rats. Mesterolone did not affect the head twitch response after 5-hydroxytryptophan in mice and was inactive in the behavioral despair test in rats. The results indicate that the psychopharmacological profile of mesterolone only slightly resembles the profile of classical imipramine-like anti-depressants.
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PMID:Psychopharmacological profile of mesterolone. 719 78


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