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，有一个渗透敏感的神经回路，连接了层膜末端（OVLT），中位前核（MNPO）和上型核的有机血管，并提出该电路控制加压素和氧蛋白释放。我们检查了渗透受体复合物是否在控制饮酒中起作用。将插管植入了雄性大鼠的OVLT，MNPO或儿子中，并测量了在10分钟内醉酒的水量（0.2MU1）的等渗或高渗CSF（0.2MU1）的影响。发现进入OVLT，MNPO或儿子的高渗CSF诱导饮酒。然后将大鼠剥夺15小时的水，并测试利多卡因注射到每个大脑区域的作用。 OVLT，MNPO或儿子活动的利多卡因块在恢复自由进入水后，在前10分钟内减少了醉酒的水量。这些结果表明，连接OVLT，MNPO和SON的渗透敏感神经回路在饮用的渗透控制以及加压素释放中起作用。旁腔内核核对血管生成素II（AII（AII）的次生源性效应的重要性已显示出（Gutman等人）（Gutman等人）（Gutman等人，1988年）。因此，我们试图调查儿子是否也参与了口渴的中央AII控制。 10^<-6> m aii的显微注射（0.2mu1）显着增加了水杆。但是，将10^<-4> m saralasin（AII拮抗剂）的显微注射不影响15小时水分的大鼠的水摄入量。因此得出的结论是，儿子中的血管紧力机制在饮用水中不起作用。