Sladek C D, Olschowka J A
Department of Physiology, University of Health Sciences/Chicago Medical School, IL 60064.
Brain Res. 1994 Aug 1;652(2):207-15. doi: 10.1016/0006-8993(94)90229-1.
Dehydration induces Fos expression and increases the length of the vasopressin (VP) mRNA poly-A tail and the content of VP mRNA in the supraoptic (SON) and paraventricular nuclei (PVN) of the hypothalamus. The current studies were performed to evaluate the effect of aging on these responses. Fischer 344 rats of 4, 14, and 28-30 months of age were either water deprived for 72 h or allowed ad libitum access to water. Fos induction in the SON and PVN was examined by immunocytochemistry in order to provide an index of cellular activation. VP mRNA content and size was examined in SON by Northern analysis as an index of VP synthetic capacity. Dehydration induced the expected increase in plasma osmolality in all three ages, however, serum VP was only increased in the 4- and 14-month-old rats. The increase in serum VP was accompanied by a decrease in VP content of the posterior pituitary (PP) in the dehydrated 4- and 14-month-old rats. PP VP content was reduced in both the hydrated and dehydrated old rats relative to the other ages (P = 0.0007). Fos was induced in both SON and PVN of all water deprived rats regardless of age. The density of Fos staining was increased in both nuclei following dehydration (SON, P = 0.002; PVN, P = 0.0001). There was also a significant increase in the number of cells expressing Fos in both nuclei in the dehydrated animals (SON, P = 0.002; PVN, P = 0.0056). There was no significant effect of age on the density of Fos staining. In contrast, dehydration failed to elicit the expected increase in VP mRNA size and content in the SON of the aged dehydrated rats although both of these parameters were increased in the 4- and 14-month-old rats (P < 0.05). Thus, the inability of old Fischer rats to increase serum VP during chronic dehydration is not caused by decreased activation of the neurons (as indicated by Fos induction), but apparently reflects depletion of PP stores of VP due to an inability to increase the amount of VP mRNA available for translation.
脱水可诱导Fos表达,并增加下丘脑视上核(SON)和室旁核(PVN)中血管加压素(VP)mRNA的多聚腺苷酸尾长度以及VP mRNA的含量。进行当前这些研究以评估衰老对这些反应的影响。将4、14以及28 - 30月龄的Fischer 344大鼠禁水72小时或随意饮水。通过免疫细胞化学检测SON和PVN中的Fos诱导情况,以提供细胞活化指标。通过Northern印迹分析检测SON中VP mRNA的含量和大小,作为VP合成能力的指标。脱水在所有三个年龄段的大鼠中均诱导了预期的血浆渗透压升高,然而,血清VP仅在4月龄和14月龄大鼠中升高。脱水的4月龄和14月龄大鼠血清VP升高的同时,垂体后叶(PP)中VP含量降低。相对于其他年龄段,水合及脱水老龄大鼠的PP VP含量均降低(P = 0.0007)。所有禁水大鼠的SON和PVN中均诱导了Fos,无论年龄大小。脱水后两个核中Fos染色密度均增加(SON,P = 0.002;PVN,P = 0.0001)。脱水动物两个核中表达Fos的细胞数量也显著增加(SON,P = 0.002;PVN,P = 0.0056)。年龄对Fos染色密度无显著影响。相比之下,尽管4月龄和14月龄大鼠中这两个参数均升高(P < 0.05),但脱水未能在老龄脱水大鼠SON中引发预期的VP mRNA大小和含量增加。因此,老龄Fischer大鼠在慢性脱水期间无法增加血清VP并非由神经元活化降低(如Fos诱导所示)所致,而是显然反映了由于无法增加可用于翻译的VP mRNA量导致PP中VP储备耗竭。