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. Author manuscript; available in PMC: 2010 Aug 1.
Published in final edited form as: J Neurochem. 2009 Jun 22;110(4):1363–1376. doi: 10.1111/j.1471-4159.2009.06229.x

Figure 7. GIRK-channel dependent inhibition of release by GABAB receptors.

Figure 7

The Ca2+ dependent release was calculated by subtracting the release obtained during a 5 min period of depolarization at 200 nM free [Ca2+] from release at 1.33 mM CaCl2. The Ca2+-dependent release of glutamate was evoked by 30 mM KCl at 1.3 mM CaCl2 (A) or by 10 mM KCl at 0.5 mM CaCl2 (C) in the absence (control) and presence of agonists and antagonists added at the indicated times prior to depolarization (arrows). Baclofen (20µM, 40s); tertiapin-Q (100 nM, 60s); ω-CgTx-GVIA (2µM, 100s) and ω-Aga-IVA (200 nM, 100s). B and D histograms show the % inhibition of Ca2+-dependent release after a 5 min depolarization under the aforementioned conditions, both in the presence of 30 mM KCl plus 1.3 mM CaCl2 (B), or 10 mM KCl plus 0.5 mM CaCl2 (D). Data represent the mean ± SEM (n=3–5). NSp>0.05; *p<0.05; **p<0.01; ***p<0.001 (students t-test) when compared with control values, unless indicated otherwise.