Lin N, Hubbard J I
Department of Physiology, University of Otago Medical School, Dunedin, New Zealand.
Brain Res Bull. 1992 May;28(5):769-74. doi: 10.1016/0361-9230(92)90258-y.
We tested a report that atrial natriuretic peptide (ANP) injected into, or near, the subfornical organ (SFO) will reduce the water consumption of previously water deprived rats and that suggested ANP acts on neurons in the SFO to bring about this action. We tested this suggestion and the hypothesis that the SFO is involved in the facilitation of drinking produced by opioids. ANP (5 nmol in 4 microliters, IVT) or naloxone (2 mg/ml/kg, SC, or 200 micrograms in 2 microliters, IVT) when given to rats deprived of water for 16 h (SC treatment) or 23 h (IVT treatment) significantly depressed postdeprivation drinking measured at 15 and 60 min. Rats with complete, partial, or control lesions of the SFO, after the same treatment, also showed a significant depression of postdeprivation drinking and, after 23-h deprivation, a significant hyperdipsia. There was no interaction between drug effects and lesion effects (two-factor analysis of variance, Tukey's post-hoc tests). The hyperdipsia declined exponentially and was lost 45-50 days after lesioning. Our results do not support the hypothesis that the SFO is involved in the actions of ANP or of opioids on postdeprivation drinking.
我们测试了一份报告，该报告称，将心房利钠肽（ANP）注入穹窿下器（SFO）或其附近，会减少先前缺水大鼠的饮水量，这表明ANP作用于SFO中的神经元以产生这种作用。我们对这一说法以及SFO参与促进阿片类药物引起的饮水这一假设进行了测试。当给缺水16小时（皮下注射治疗）或23小时（脑室内注射治疗）的大鼠注射ANP（4微升中含5纳摩尔，脑室内注射）或纳洛酮（2毫克/毫升/千克，皮下注射，或2微升中含200微克，脑室内注射）时，在15分钟和60分钟时测量的缺水后饮水显著减少。在相同处理后，SFO完全、部分或对照损伤的大鼠也表现出缺水后饮水显著减少，并且在缺水23小时后出现显著的饮水过多。药物效应和损伤效应之间没有相互作用（双因素方差分析，Tukey事后检验）。饮水过多呈指数下降，并在损伤后45 - 50天消失。我们的结果不支持SFO参与ANP或阿片类药物对缺水后饮水作用的假设。
