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. 2010 May 13;21(1):212–221. doi: 10.1093/cercor/bhq081

Figure 6.

Figure 6.

β and α2 receptors activation increase GABA release in LII/III-eIPSCs. LII/III-eIPSCs amplitude time courses and averages showing the effects of adrenergic agonists and antagonists. (A) The antagonists for β and α2 receptors (propranolol and yohimbine) blocked the enhancement of the LII/III-eIPSCs by NE, unmasking a NE-induced amplitude decrease. (B) Prazosin does not block the enhancement of the eIPSCs by NE. (C) The selective β noradrenergic receptor agonist (isoproterenol, iso 50 μM) increases LII/III-eIPSCs amplitude. (D) The β antagonist propranolol (1 μM) blocks the effect of isoproterenol. (E) The α2 agonist clonidine (1 μM) mimics the NE effects on eIPSCs in 28% of the cells studied. (F) Effects of clonidine were blocked by previous application of the α2 antagonist yohimbine (1 μM). (G) Application of the α1 agonist phenylephrine (1 μM) decreases eIPSCs amplitude. Complete statistics are reported in the text. (H) Summary of the experiment with adrenergic agonists and antagonists on eIPSCs evoked from LII/III stimulation. These results suggest that β and α2 receptors are responsible for NE–induced eIPSCs enhancement.