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Long-term antidepressant treatments alter 5-HT2A and 5-HT2C receptor-mediated hyperthermia in Fawn-Hooded rats.

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We have recently demonstrated that hyperthermia induced by 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and m-chlorophenylpiperazine (m-CPP) are separately mediated by selective stimulation of 5-HT2A and 5-HT2C receptors, respectively in Wistar rats. Furthermore, hyperthermia induced by

Whole-body hyperthermia and a subthreshold dose of citalopram act synergistically to induce antidepressant-like behavioral responses in adolescent rats.

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Open and randomized, double blind, placebo-controlled clinical trials have demonstrated clinical efficacy of infrared whole-body hyperthermia in treatment of major depressive disorder (MDD). Demonstration of antidepressant-like behavioral effects of whole-body hyperthermia in preclinical rodent

Involvement of a central alpha-adrenoceptor system in antidepressant potentiation of hyperthermia induced by thyrotropin releasing hormone.

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Thyrotropin releasing hormone (TRH) causes hyperthermia in mice which is potentiated by tricyclic antidepressants (nortriptyline, imipramine, clomipramine, amitriptyline), the monoamine oxidase inhibitor, tranylcypromine, and various other antidepressants (maprotiline, nomifensin, viloxazine). Only

Evaluation of AaDOP2 receptor antagonists reveals antidepressants and antipsychotics as novel lead molecules for control of the yellow fever mosquito, Aedes aegypti.

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The yellow fever mosquito, Aedes aegypti, vectors disease-causing agents that adversely affect human health, most notably the viruses causing dengue and yellow fever. The efficacy of current mosquito control programs is challenged by the emergence of insecticide-resistant mosquito populations,

Hyperthermia induced by m-CPP in the rat and its modification by antidepressant treatments.

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Administration of the serotonin agonist m-chlorophenylpiperazine to rats produced a dose-related hyperthermia. Pretreatment with the serotonin receptor antagonist metergoline totally abolished this response, whereas similar treatment with haloperidol, phenoxybenzamine, naloxone, clonidine, pindolol,

Use of potentiation of thyrotrophin releasing hormone (TRH)-induced hyperthermia as a test for screening antidepressants which activate alpha-adrenoceptor systems.

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1 The minimal dose which significantly potentiates the hyperthermia induced by thyrotrophin releasing hormone (TRH, 40 mg/kg i.p.) in mice has been established for tricyclic and other antidepressants (imipramine, amitriptyline, clomipramine, nortriptyline, maprotiline, nomifensine, viloxazine)

Adaptive and differential changes on beta- and alpha 2-adrenoreceptors mediated hyperthermia after chronic treatment with antidepressant drugs in the rat kept at high ambient temperature.

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We found previously that the beta-agonist clenbuterol and the alpha-agonist clonidine produced hyperthermia in rats kept at high ambient temperature, which effects were mediated by beta- and alpha 2-adrenoceptors, respectively. In the present paper this observation was used for testing the

The effect of repeated treatment with antidepressant drugs on the thyrotropin-releasing hormone (TRH)-induced hyperthermia in mice.

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The effect of acute (single dose) or repeated (twice daily, for 14 days) administration of 10 mg kg-1 p.o. of imipramine, amitriptyline, citalopram or mianserin has been examined on the hyperthermia induced by thyrotropin-releasing hormone (TRH) (40 mg kg-1 i.p., 2, or 2 and 72 h after single or

mGlu2/3 agonist-induced hyperthermia: an in vivo assay for detection of mGlu2/3 receptor antagonism and its relation to antidepressant-like efficacy in mice.

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An assay to detect the on-target effects of mGlu2/3 receptor antagonists in vivo would be valuable in guiding dosing regimens for the exploration of biological effects of potential therapeutic import. Multiple approaches involving blockade of mGlu2/3 receptor agoinist-driven behavioral effects in

Hyperthermia complicating tricyclic antidepressant overdose.

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We observed a 51-year-old woman who was admitted for severe amitriptyline overdose. Besides major cardiovascular complications, the patient developed severe hyperpyrexia with a central body temperature of more than 43 degrees C for 5 h. The patient died on day 3 from cardiocirculatory collapse and

A fatal case of hyperthermia due to tricyclic antidepressant intoxication.

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We report here an autopsy case of a 49-year-old woman with depression who died of hyperthermia, probably due to amitriptyline intoxication. She was found dead in bed with several empty amitriptyline pill containers. Her rectal temperature was 41.5 degrees C approximately 3 hours after death. Plasma

Use of tricyclic antidepressants in a patient with malignant hyperthermia.

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[The effect of tricyclic antidepressants on rabbit 5-hydroxytryptophan hyperthermia].

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Antidepressant drug fever.

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Tricyclic antidepressants and malignant hyperthermia.

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