期刊
BRAIN RESEARCH
卷 1028, 期 2, 页码 191-202出版社
ELSEVIER
DOI: 10.1016/j.brainres.2004.09.012
关键词
thermoregulation; vasomotor symptom; 5-HT2A receptor; hot flush; estrogen; animal model
Menopause-associated thermoregulatory dysfunction, including hot flushes and night sweats, is effectively treated by hormonal therapies that include estrogens. Evidence suggests that estrogen regulates serotonin 2A (5-HT2A) receptor expression and that 5-HT2A receptors are involved in thermoregulation. Therefore, the role of 5-HT2A receptors in thermoregulation was assessed in two rat models of ovarjectomyinduced thermoregulatory dysfunction. The first model is based on measurement of the tail-skin temperature (TST) increase following naloxone-induced withdrawal in morphine-dependent ovariectomized (OVX) rats (MD model), while the second model relies on telemetric assessment of diumal TST changes in ovariectornized rats (telemetry model). Treatment with a 5-HT2A/2c receptor agonist, (+2,5dimethoxy-4-iodoamphetamine hydrochloride (DOI), prevented the naloxone-induced TST increase in the MD model and restored normal active-phase TST in the telemetry model. The selective 5-HT2A receptor antagonist, MDL-100907, had no effect on the naloxone-induced flush when administered alone in the MD model, but it decreased DOI's ability to abate the flush. In the telemetry model, MDL-100907 attenuated the DOI-induced decrease in active-phase TST. Interestingly, MDL-100907 increased TST in both models when given alone, with the TST increase occurring prior to the naloxone-induced flush in the MD model. To evaluate the role of central nervous system (CNS) 5HT(2A) receptors in TST regulation, DOI was administered in combination with a known peripheral 5-HT2A/2c receptor antagonist, xylamidine, in the MD model. Xylamidine had no effect on DOI's ability to abate the naloxone-induced flush. These results indicate that activation of central 5-HT2A receptors restores temperature regulation in two rodent models of ovariectomy-induced thernioregulatory dysfunction. (C) 2004 Elsevier B.V. All rights reserved.
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