Departmental Bulletin Paper 正中視索前核へのグルタミン酸およびGABA受容体機構による脳弓下器官でのアンギオテンシンII受容によって誘発される飲水行動の調節
セイチュウ シサク ゼンカク エノ グルタミンサン オヨビ GABA ジュヨウタイ キコウ ニヨル ノウキュウ カキカン デノ アンギオテンシンII ジュヨウ ニヨッテ ユウハツ サレル インスイ コウドウ ノ チョウセツ
Glutamatergic and GABAergic Mechanisms in the Median Preoptic Nucleus Modulate the Water Intake Induced by Angiotensin II Acting at the Subfornical organ in Rats

田中, 淳一  ,  高橋, 眞琴

32pp.449 - 453 , 2017-03-10 , 鳴門教育大学 , Naruto University of Education
The subfornical organ (SFO), a circumventricular structure lacking the normal blood−brain barrier, is a target site of circulating angiotensin II (ANG II) for elicitation of drinking and pressor responses. The SFO sends glutamatergic, γ−aminobutyric acid (GABA) ergic and angiotensinergic fibers to the median preoptic nucleus (MnPO).The present study was carried out to clarify whether glutamatergic and GABAergic receptor mechanisms in the MnPO participate in the modulation of drinking response elicited by ANG II activation of the SFO. The effects of petreatment with the N−methyl−D−asparatate (NMDA), non−NMDA, GABAA, and GABAB receptor antagonists in the MnPO on the drinking response caused by microinjections of ANG II into the SFO were examined. Prior injections of either dizocilpine (MK801), a NMDA antagonist, or6−cyano−7−nitroquinoxaline−2, 3−dion (CNQX), a non−NMDA antagonist, significantly reduced the ANG II−induced water ingestion, indicating that the glutamatergic receptor system in the MnPO may serve to enhance or maintain of the drinking behavior in response to the SFO inputs activated by circulating ANG II. Pretreatment with either the GABAA antagonist bicuculine methiodide or the GABAB antagonist phaclofen in the MnPO significantly increased the water intake caused by ANG II injected into the SFO, showing the inhibitory action of GABAergic receptor mechanisms on drinking responses to the SFO inputs activated by ANG II. These findings provide the evidence for involvement of both glutamatergic and GABAergic receptor mechanisms are implicated in the modulation of water intake caused by ANG II acting at the SFO.

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