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In this study, using whole cell recording from retrogradely labeled PVN neurons in rat brain slices, we determined the signaling mechanisms responsible for the effect of Ang II on synaptic GABA release to spinally projecting PVN neurons. Bath application of Ang II reproducibly decreased the frequency of GABAergic miniature postsynaptic inhibitory currents (mIPSCs) in fluorescence-labeled PVN neurons. Ang II failed to change the frequency of mIPSCs in labeled PVN neurons treated with pertussis toxin. However, Ang II\u2013induced inhibition of mIPSCs persisted in the presence of either CdCl<jats:sub>2<\/jats:sub>, a voltage-gated Ca<jats:sup>2+<\/jats:sup>channel blocker, or 4-aminopyridine, a blocker of voltage-gated K<jats:sup>+<\/jats:sup>channels. Interestingly, inhibition of superoxide with superoxide dismutase or Mn(III) tetrakis (4-benzoic acid) prophyrin completely blocked Ang II\u2013induced decrease in mIPSCs. By contrast, inhibition of hydroxyl radical formation with the ion chelator deferoxamine did not significantly alter the effect of Ang II. These findings suggest that the presynaptic action of Ang II on synaptic GABA release in the PVN is mediated by the pertussis toxin\u2013sensitive G<jats:sub>i\/o<\/jats:sub>proteins but not by voltage-gated Ca<jats:sup>2+<\/jats:sup>and K<jats:sup>+<\/jats:sup>channels. Ang II attenuates GABAergic input to PVN presympathetic neurons through reactive oxygen species, especially superoxide anions.<\/jats:p>","DOI":"10.1152\/jn.01329.2006","type":"journal-article","created":{"date-parts":[[2007,2,8]],"date-time":"2007-02-08T01:41:55Z","timestamp":1170898915000},"page":"3279-3287","source":"Crossref","is-referenced-by-count":53,"title":["Signaling Mechanisms of Angiotensin II\u2013Induced Attenuation of GABAergic Input to Hypothalamic Presympathetic 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