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The effects of hormone replacement therapy on hypothalamic neuropeptide gene expression in a primate model of menopause.
Abel TW, Voytko ML, Rance NE
(1999) J Clin Endocrinol Metab 84: 2111-8
MeSH Terms: Animals, Carboxylic Ester Hydrolases, Estrogen Replacement Therapy, Female, Hypothalamus, In Situ Hybridization, Macaca fascicularis, Menopause, Microglia, Models, Biological, Neurokinin B, Neurons, Oligonucleotide Probes, Ovariectomy, Pro-Opiomelanocortin
Show Abstract · Added March 5, 2014
Menopause is associated with increased neurokinin B (NKB) gene expression and decreased proopiomelanocortin (POMC) gene expression in the human hypothalamus. In the present study, young, ovariectomized cynomolgus monkeys were used in a model of menopause to examine the effects of hormone replacement therapy (HRT) on hypothalamic neuropeptide gene expression. A secondary goal was to determine whether HRT produces signs of estrogen toxicity in the primate hypothalamus by examining POMC neurons and microglial cells. In situ hybridization was performed using synthetic, radiolabeled, 48-base oligonucleotide probes. Alpha-napthyl butyrate esterase histochemistry was used to visualize microglial cells. Both estrogen and estrogen plus progesterone treatments produced a marked suppression of the number of infundibular neurons expressing NKB gene transcripts. In contrast, HRT had no effect on the POMC system of neurons or the number of microglial cells in the infundibular nucleus. These results provide strong support for the hypothesis that the increased NKB gene expression in the hypothalamus of postmenopausal women is secondary to estrogen withdrawal. Conversely, these data suggest that the dramatic decline in the numbers of neurons expressing POMC gene transcripts in older women is caused by factors other than ovarian failure. Finally, we found no evidence that HRT, in doses designed to mimic currently prescribed regimens, produces signs of estrogen toxicity in the primate infundibular nucleus.
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Plasma extravasation in the rat trachea induced by cold air is mediated by tachykinin release from sensory nerves.
Yoshihara S, Chan B, Yamawaki I, Geppetti P, Ricciardolo FL, Massion PP, Nadel JA
(1995) Am J Respir Crit Care Med 151: 1011-7
MeSH Terms: Air, Animals, Cold Temperature, Evans Blue, Extravasation of Diagnostic and Therapeutic Materials, Neurokinin B, Neurons, Afferent, Parainfluenza Virus 1, Human, Rats, Rats, Inbred F344, Respiration, Artificial, Trachea, Tracheitis, Virus Diseases
Show Abstract · Added March 5, 2014
Cold air was delivered to anesthetized, artificially ventilated, pathogen-free F344 rats via a tracheal cannula. Inhalation of cold air increased Evans blue dye extravasation in the trachea in a time-dependent (1 to 10 min) manner. Plasma extravasation increased after 3 min exposure to cold air and reached a maximum after 10 min exposure. The neutral endopeptidase inhibitor, phosphoramidon (2.5 mg/kg, intravenously), increased by 84% the plasma extravasation induced by inhalation of cold air for 1 min. The plasma extravasation evoked by 5 min exposure to cold air was abolished by the NK1 tachykinin receptor antagonist, CP-99,994 (4 mg/kg, intravenously); was reduced 30% by the B2 bradykinin receptor antagonist, HOE140 (0.1 mumol/kg, intravenously); and was not affected by H1 (pyrilamine, 10 mg/kg, intraperitoneally) or H2 (cimetidine, 10 mg/kg, intraperitoneally) histamine receptor antagonists or the cyclooxygenase inhibitor indomethacin (5 mg/kg, intravenously). In rats infected with Sendai virus, plasma extravasation evoked by inhalation of cold air was greater than in pathogen-free rats. Pretreatment with CP-99,994 (4 mg/kg, intravenously) inhibited completely the plasma extravasation induced by cold air in virus-infected rats. These findings indicate that cold air increases plasma extravasation in the rat trachea by a neurogenic mechanism that involves the release of tachykinins from sensory nerves. Kinin release may also play a role in this neurogenic inflammatory response.
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14 MeSH Terms