Rowland N E, Fregly M J, Han L, Smith G
Department of Psychology and Physiology, University of Florida, Gainesville 32611-2250, USA.
Brain Res. 1996 Jul 22;728(1):90-6.
Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats. In the first experiment, rats were depleted of sodium by treatment with furosemide 24 h prior to sacrifice and without access to either food or sodium solution. Some rats had access to distilled water, and others had no fluids available during the 24 h. All of the furosemide-treated rats showed Fos-IR in both the subfornical organ (SFO) and around the organum vasculosum laminae terminalis (OVLT). Rats with access to distilled water during the depletion period showed no Fos-IR in the supraoptic (SON) or paraventricular hypothalamic nuclei (PVN) and, in parallel behavioral studies, comparably-treated rats consumed only 0.3 M NaCl solution at the end of the 24 h. In rats that had no fluids during the deprivation period, only about one half showed Fos-IR in SON and PVN and, in parallel behavioral studies, comparably treated rats consumed both water and 0.3 M NaCl solution at the end of 24 h. In a second experiment, cerebroventricular administration of renin stimulated short latency intake of 0.3 M NaCl and water. The relative intakes of water and NaCl were comparable at a low dose of renin, but intake of water exceeded that of NaCl after higher doses. Renin induced Fos-IR in SFO, MnPO, peri-OVLT region, SON and PVN. Both Fos-IR and fluid intake were antagonized by administration of losartan, an angiotensin II type 1 receptor antagonist. Thus, only the circumventricular organs of the lamina terminalis showed Fos-IR during each natriorexigenic regimen in these studies. These data support the view that Ang II of both central and peripheral origin activates the SFO and/or peri-OVLT region and contributes to sodium appetite.
进行了两项实验，以研究大鼠脑中钠食欲的表达与Fos样免疫反应性（Fos-IR）出现之间的关系。在第一个实验中，在处死前24小时用速尿处理大鼠以耗尽其体内的钠，且不给它们提供食物或钠溶液。一些大鼠可以获得蒸馏水，而另一些大鼠在这24小时内没有任何液体供应。所有经速尿处理的大鼠在穹窿下器官（SFO）和终板血管器（OVLT）周围均显示出Fos-IR。在耗尽期能获得蒸馏水的大鼠，其视上核（SON）或下丘脑室旁核（PVN）未显示Fos-IR，并且在平行的行为学研究中，经相同处理的大鼠在24小时结束时仅饮用0.3M NaCl溶液。在剥夺期没有液体供应的大鼠中，只有约一半在SON和PVN中显示出Fos-IR，并且在平行的行为学研究中，经相同处理的大鼠在24小时结束时既饮水又饮用0.3M NaCl溶液。在第二个实验中，脑室内注射肾素刺激了对0.3M NaCl和水的短潜伏期摄取。在低剂量肾素时，水和NaCl的相对摄取量相当，但在高剂量后，水的摄取量超过了NaCl。肾素在SFO、中脑导水管周围灰质（MnPO）、OVLT周围区域、SON和PVN中诱导了Fos-IR。给予1型血管紧张素II受体拮抗剂氯沙坦可拮抗Fos-IR和液体摄取。因此，在这些研究中，在每种致钠食欲的方案中，只有终板的室周器官显示出Fos-IR。这些数据支持这样的观点，即中枢和外周来源的血管紧张素II均激活SFO和/或OVLT周围区域，并促成钠食欲。
