Serotonin 2A receptors modulate tail-skin temperature in two rodent models of estrogen deficiency-related thermoregulatory dysfunction

Sipe, Kimberly J.; Leventhal, Liza; Burroughs, Kevin D.; Cosmi, Scott; Johnston, Grace H.; Deecher, Darlene C.

doi:10.1016/j.brainres.2004.09.012

Cited by 58 publications

(56 citation statements)

References 26 publications

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“…Data from ovariectomized rats indicated that a 5-HT 2A agonist restores temperature regulation of induced thermoregulatory dysfunction (Lin, Tsay, Su, & Chueh, 1998;Sipe et al, 2004). There is a relationship between serum serotonin levels and the severity of menopausal symptoms (Slopien, Meczekalski, & Warenik-Szymankiewicz, 2003).…”

Section: Gluconeuroendocrinementioning

confidence: 99%

Physiology and Endocrinology of Hot Flashes in Prostate Cancer

Engstrom

Kasper

2007

Am J Mens Health

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Section: Gluconeuroendocrinementioning

confidence: 99%

Physiology and Endocrinology of Hot Flashes in Prostate Cancer

Engstrom

Kasper

2007

Am J Mens Health

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“…Activation of 5-HT 2A receptors has been reported to induce hyperthermia which can be blocked by 5-HT 2A receptor antagonists in rodents [18, 19]. The involvement of 5-HT 2A receptors in the modulation of peripheral temperature by measuring changes in tail-skin temperature (TST) in ovariectomized (OVX) rats has been previously reported [20, 21]. Chronic administration of the 5-HT 2A/2C receptor antagonist, mirtazapine (10 mg/ kg i.p.…”

Section: Introductionmentioning

confidence: 99%

“…), alleviated OVX-induced temperature dysregulation in a telemetry-based rat model [20]. Acute administration of the 5-HT 2A/2C receptor agonist, (–)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI), also resulted in alleviation of temperature dysfunction in the same model [21]. Thus, activation as well as blockade of 5-HT 2A/2C receptors has been reported to impact temperature regulation.…”

Section: Introductionmentioning

confidence: 99%

“…Two distinct rodent models were used to evaluate the effect of FLX on TST. The first model is a physiologically (OVX) induced thermoregulatory dysfunction telemetric model that depends on estrogen’s regulation of diurnal TST [21, 24, 25]. The second model used in this study is a pharmacological model that relies on a naloxone- induced increase in TST in morphine-dependent (MD) OVX rats [21, 25, 26].…”

Section: Introductionmentioning

confidence: 99%

“…The first model is a physiologically (OVX) induced thermoregulatory dysfunction telemetric model that depends on estrogen’s regulation of diurnal TST [21, 24, 25]. The second model used in this study is a pharmacological model that relies on a naloxone- induced increase in TST in morphine-dependent (MD) OVX rats [21, 25, 26]. The pharmacologically induced (opiate antagonism) acute increase in TST (artificial flush) and the physiologically induced (OVX-induced) dual model approach were used since skepticism has been raised regarding the ‘classic’ MD model [26, 27] and its relevance to vasomotor disturbances and thermoregulatory dysfunction [20].…”

Section: Introductionmentioning

confidence: 99%

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The Role of the Selective Serotonin Reuptake Inhibitor Fluoxetine in Temperature Regulation in Ovariectomized Rat Models

et al. 2006

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Thermoregulation is an integrated network of neuroendocrine, autonomic and somatosensory responses. Thermoregulatory dysfunction occurs during fluctuations or decline of gonadal hormone levels and results in vasomotor symptoms such as hot flushes and/or night-time sweating. The neurotransmitter serotonin (5-HT), has been reported to play a role in thermoregulation via changes in extracellular 5-HT levels and/or activation of various 5-HT receptors. The purpose of this study was to evaluate the role of the selective 5-HT reuptake inhibitor (SSRI), fluoxetine (FLX), on temperature regulation using ovariectomized (OVX) rodent models of thermoregulation. Single, subcutaneous (s.c.) administration of FLX (3, 10, 30 and 60 mg/kg) dose-dependently reduced core body temperature (CBT). FLX at 3 and 10 mg/kg s.c. showed no statistically significant decrease on tail-skin temperature (TST), whereas at higher doses (30 and 60 mg/kg) a significant decrease in TST was noted in the telemetry model. To mimic chronic SSRI treatment, a 5-HT_1A antagonist (WAY-100635; 0.3 mg/kg) was administered 20 min prior to FLX (10 mg/kg). This combination showed no significant improvement on temperature dysfunction compared to FLX alone. Similarly, in a morphine-dependent model of temperature dysfunction FLX, was inactive at 10 mg/kg whereas the 30 and 60 mg/kg s.c. dose abated the naloxone-induced increase in TST by 55 and 81%, respectively. In summary, FLX affected CBT at all doses, but alleviated thermoregulatory dysfunction only at higher doses that are non-selective for the 5-HT system.

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