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Institute of Physiology, Faculty of Medicine (Charité), Humboldt University, Tucholskystr. 2, 10117 Berlin, Germany
1Correspondence: Institute of Physiology, Faculty of Medicine (Charité), Humboldt University Berlin, Tucholskystr. 2, 10117 Berlin, Germany. E-mail: doris.albrecht{at}charite.de
The effects of iontophoretically ejected angiotensin II (Ang II) on the
firing rate of neurons in the basolateral complex and the central and
cortical amygdala were investigated in two strains of urethane
anesthetized rats. In normotensive Sprague-Dawley rats, Ang II induced
a significant increase in the discharge rate of responsive amygdaloid
neurons. In contrast, in the hypertensive transgenic [TGR(mREN-2)27]
rats with higher brain Ang II level, Ang II more often caused
inhibitory effects on the amygdaloid firing rate in comparison with
controls. The distribution of nonresponsive, excited, and inhibited
neurons differed significantly in the two rat strains. Moreover, the
responsiveness of amygdaloid neurons was significantly higher in
transgenic rats in comparison with controls. Both the increase and the
decrease in the firing rate caused by Ang II could be blocked either by
angiotensin AT1 or by AT2 receptor-specific
antagonists. In many cases, the Ang II-induced decrease in the firing
rate was antagonized by bicuculline, a
-aminobutyric acid
(GABAA) antagonist. The higher responsiveness of amygdaloid
neurons in transgenic rats as well as the predominance of inhibitory
effects, presumedly mediated by GABAergic interneurons, could change
the output of the amygdala and its influence on thirst, kidney, and
cardiovascular function or on processes of learning and
anxiety.Albrecht, D., Nitschke, T., and Von Bohlen und Halbach, O.
Various effects of angiotensin II on amygdaloid neuronal activity in
normotensive control and hypertensive transgenic [TGR(mREN-2)27]
rats.
Key Words: amygdala angiotensin II AT1 AT2 bicuculline extracellular recording urethane iontophoresis
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