Angiotensin II inhibits long-term potentiation within the lateral nucleus of the amygdala through AT1 receptors

被引：58
|
作者：
von Bohlen und Halbach, O [1 ]
Albrecht, D [1 ]
机构：
[1] Humboldt Univ, Fac Med Charite, Inst Physiol, D-10117 Berlin, Germany
来源：
PEPTIDES | 1998年 / 19卷 / 06期
关键词：
long-term potentiation; amygdala; angiotensin II; rats; in vitro; extracellular;
D O I：
10.1016/S0196-9781(98)00044-8
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Long-term potentiation (LTP) of field potentials in the lateral nucleus of the amygdala (LA) evoked by brief tetanic stimuli of the LA were observed in horizontal rat brain slices. The amplitude of field potentials was significantly enhanced after repetitive stimulation. When angiotensin II was administrated the induction of LTP was suppressed. This inhibition of LTP was mediated by angiotensin II because it could be blocked by the coadministration of saralasin, an nonspecific angiotensin II antagonist. The coadministration of losartan, a competitive antagonist of the AT, receptor subtype, concomitant with angiotensin II was also able to block this inhibition. The coadministration of the AT, receptor antagonist PD 123,319 failed to block the inhibition of LTP. (C) 1998 Elsevier Science Inc.
引用
收藏
页码：1031 / 1036
页数：6
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