Osmotic regulation of estrogen receptor-beta expression in magnocellular vasopressin neurons requires lamina terminalis.
Osmotic regulation of estrogen receptor-beta expression in magnocellular vasopressin neurons requires lamina terminalis.
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大细胞加压素神经元中雌激素受体β表达的渗透调节需要终板。
DOI：
10.1152/ajpregu.00478.2003
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Sladek,CeliaD
中科院分区：
文献类型：
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作者：
Somponpun,SuwitJ;Johnson,AlanKim;Beltz,Terry;Sladek,CeliaD
大鼠视上核和室旁核（SON和室旁核）大细胞加压素（VP）神经元雌激素受体β（ER β）表达在2%NaCl染毒72 h后消失。为了检验起源于终板血管器（OVLT）区域的神经敏感机制控制SON和PVN中ER-β表达的假设，在腹侧第三脑室（AV 3V）前部区域进行电解损伤后，将动物禁水。这种损伤阻止VP释放的渗透刺激。手术后4周，雄性大鼠[病变组（n= 16）或假手术组（n= 14）]被禁水48小时或允许自由饮水。水剥夺可抑制SON和PVN大细胞内ER-β免疫反应性（-ir）的表达。Fos-ir在这些神经元中是明显的，血浆渗透压（Posm）和红细胞压积（Ht）与假水化大鼠相比显著升高（Posm，304 ± 1 vs.318 ± 2 mosmol/kgH 2 O;P< 0.001; Ht，49.6 ± 0.6 vs.55.0 ± 0.9%;P< 0.001）。ER-β表达在假水合、AV 3V水合和8只AV 3V脱水大鼠中的6只中相当，尽管两组的Posmin显著增加（AV 3V水合，312 ± 2; AV 3V脱水，380 ± 10 mosmol/kgH 2 O;P< 0.001）。ER-β耗竭的AV 3V脱水大鼠不进行OVLT消融。尽管Posm值升高，但AV 3V水合动物的SON中Fos-ir较低或检测不到。在AV 3V脱水大鼠中，Fos-ir显著低于假脱水动物，但与假水合组相比显著增加。这可能反映了不抑制ER-β表达的非渗透参数的激活。这些数据支持这样的假设，即通过渗透刺激抑制SON中的ER-β表达是由终板中的神经元介导的。
Estrogen receptor-β (ER-β) expression in rat magnocellular vasopressin (VP) neurons of the supraoptic and paraventricular nuclei (SON and PVN, respectively) becomes undetectable after 72 h of 2% NaCl consumption. To test the hypothesis that osmosensitive mechanisms that originate in the region of the organum vasculosum lamina terminalis (OVLT) control ER-β expression in the SON and PVN, animals were water deprived after electrolytic lesions were performed on the area anterior to the ventral third ventricle (AV3V). Such lesions prevent osmotic stimulation of VP release. Four weeks after surgery, male rats [lesioned (n= 16) or sham (n= 14)] were water deprived for 48 h or allowed water ad libitum. Water deprivation eliminated ER-β-immunoreactivity (-ir) in SON and magnocellular PVN of sham-lesioned animals. Fos-ir was evident in these neurons, and plasma osmolality (Posm) and hematocrit (Ht) were significantly elevated compared with the sham-hydrated rats (Posm, 304 ± 1 vs. 318 ± 2 mosmol/kgH2O;P< 0.001; Ht, 49.6 ± 0.6 vs. 55.0 ± 0.9%;P< 0.001). ER-β expression was comparable in sham-hydrated, AV3V-hydrated, and 6 of 8 AV3V-dehydrated rats despite significant increases in Posmin both groups (AV3V hydrated, 312 ± 2; AV3V dehydrated, 380 ± 10 mosmol/kgH2O;P< 0.001). OVLT was not ablated in the AV3V-dehydrated rats in which ER-β was depleted. Fos-ir was low or undetectable in SON in the AV3V-hydrated animals despite elevated Posmvalues. In AV3V-dehydrated rats, Fos-ir was significantly less than in sham-dehydrated animals but was significantly increased compared with the sham-hydrated group. This could reflect activation by nonosmotic parameters that do not inhibit ER-β expression. These data support the hypothesis that inhibition of ER-β expression in the SON by osmotic stimulation is mediated by osmoreceptive neurons in the lamina terminalis.