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

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 AT1 receptor subtype, concomitant with angiotensin II was also able to block this inhibition. The coadministration of the AT2 receptor antagonist PD 123,319 failed to block the inhibition of LTP.