Abstract

1. In brain slice preparations from the hypothalamus of domestic ducks, single-unit activity was recorded extracellularly to investigate location and properties of angiotensin II (AngII)-responsive neurones in various periventricular regions. 2. When exposing the slice to 10(-7) M-AngII in the perfusion medium, more than 65% of the neurones recorded in the subfornical organ (SFO) were activated (49 out of 75) and none inhibited. In the magnocellular (MC) region of the paraventricular nucleus (PVN) only four out of eighty-one neurones were influenced by AngII; one was inhibited and three were activated. In the anterior third ventricle region (A3V) two out of twenty-one neurones were activated by AngII. In the dorsal periventricular (PeV) region, one out of thirty-seven neurones was activated and one inhibited. The changes in firing rate of AngII-responsive neurones at comparable doses of AngII were generally large in the SFO and A3V but were small in neurones from the MC and PeV regions. 3. Analysis of AngII-responsive SFO neurones consistently revealed a dose-dependent stimulation with a threshold at 10(-9) M-AngII. The AngII antagonist 1Sar-8Ile-AngII (4 x 10(-7) to 10(-6) M) caused reversible, complete or partial suppression of responsiveness to 10(-7) M-AngII. Synaptic blockade with a medium low in Ca2+ and high in Mg2+ did not abolish AngII responsiveness in eight out of ten SFO neurones tested. 4. Angiotensin III affected neither AngII-responsive nor AngII-insensitive neurones. When eighteen AngII-responsive neurones were exposed to hypertonic stimulation (+20 to +30 mosmol/kg) by adding NaCl to the perfusion medium, only one neurone was stimulated and two were inhibited. 5. The results indicate that: (a) the SFO is a specific target for circulating AngII; (b) although neurones in the A3V responsive to AngII are rare, the pronounced excitation of those which were found suggest that neurones in this region might serve as targets for AngII acting from the brain side; (c) neurones in the MC region do not seem to function as direct AngII targets; (d) neuronal AngII responsiveness in the duck's hypothalamus seems to be specific inasmuch as activation by AngII (i) is readily blocked by an AngII antagonist, (ii) cannot be induced by AngIII, and (iii) is not associated, as a rule, with responsiveness to hypertonic stimulation.

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