A study on the central osmoreceptor mechanism controlling drinking

中枢渗透压感受器控制饮酒机制的研究

基本信息

批准号：
03670075
负责人：
NEGORO Hideo
金额：
$ 1.34万
依托单位：
Fukui Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1992
项目状态：
已结题

项目摘要

We have demonstrated that there is an osmosensitive neural circuit connecting the organum vasculosum of the lamina terminalis(OVLT),median preoptic nucleus(MnPO)and supraoptic nucleus and suggested that the circuit controls the vasopressin and oxytocin release. We examined whether the osmoreceptor complex plays a role in control of drinking. Cannulae were implanted into the OVLT,MnPO or SON of male rats and the effects of injections(0.2mu1)of isotonic or hypertonic CSF into each of the regions on the volume of water drunk in 10 min were measured. Hypertonic CSF injected into the OVLT,MnPO or SON was found to induce drinking. The rats were then deprived of water 15 hours and tested for the effect of lidocaine injection into each of the brain regions. The lidocain block of the activity of the OVLT,MnPO or SON reduced the volume of water drunk during the first 10 min after resuming free access to water. These results suggest that the osmosensitive neural circuit connecting the OVLT,MnPO and SON plays a role in the osmotic control of drinking as well as vasopressin release.The significance of the paraventricular nucleus for the dipsogenic effect of angiotensin II(AII) has been shown(Gutman et al, 1988). So we made attempt to investigate whether or not the SON is also involved in the central AII control of thirst. The microinjection(0.2mu1)of 10^<-6>M AII into the SON significantly increased water-intake. However,the microinjection of 10^<-4>M saralasin(AII antagonist)into the SON did not influence water intake in 15 hour water-deprived rats. Thus it is concluded that the angiotensinergic mechanism in the SON does not play a role in drinking in water-deprived dehydrated rat.

我们已经证明存在一个连接终板血管器(OVLT)、正中视前核(MnPO)和视上核的渗透敏感神经回路，并表明该回路控制加压素和催产素的释放。我们检查了渗透压感受器复合体是否在控制饮酒中发挥作用。将插管植入雄性大鼠的OVLT、MnPO或SON中，并测量等渗或高渗脑脊液注射到各区域（0.2μl）对10分钟内饮水量的影响。发现将高渗脑脊液注射到 OVLT、MnPO 或 SON 中会诱导饮酒。然后让大鼠禁水 15 小时，并测试利多卡因注射到每个大脑区域的效果。 OVLT、MnPO 或 SON 活性的利多卡因阻滞剂减少了恢复自由饮水后前 10 分钟内的饮水量。这些结果表明，连接 OVLT、MnPO 和 SON 的渗透敏感神经回路在饮酒的渗透压控制以及加压素释放中发挥作用。室旁核对于血管紧张素 II (AII) 的促动力作用的重要性已被证明。古特曼等人，1988）。因此我们尝试调查SON是否也参与了中央AII对口渴的控制。将10^-6M AII微量注射(0.2μl)到SON中显着增加了水的摄入量。然而，将10^-4M萨拉拉辛(AII拮抗剂)显微注射到SON中并不影响15小时禁水大鼠的饮水量。由此得出结论，SON中的血管紧张素能机制在缺水脱水大鼠的饮水中不起作用。