Journal: The Journal of Physiology
Article Title: Inhibition of BK channels by GABAb receptors enhances intrinsic excitability of layer 2/3 vasoactive intestinal polypeptide‐expressing interneurons in mouse neocortex
doi: 10.1113/jp286439
Figure Lengend Snippet: Figure 4. BK channels suppress L2/3 VIP-IN intrinsic excitability at high extracellular Ca2+ level A, examples of firing responses of type 1 upon a 500 ms-long pulse. Lower traces show step intensities of current injected to the soma, middle traces show neuronal firings at rheobase, upper traces represent maximum spike frequency in control ACSF (Ctrl, left) and after application of the BK channel antagonist (paxilline, Pax, right). B, mean (±SD) firing frequency–current curves type 1 in control and after Pax (P < 0.05, paired t test, n = 12). C, Hill sigmoidal curves fitted to the data shown in B, n = 12. D, left, within-cell comparison and mean (±SD) maximum firing frequency of type 1 in control and after Pax (P = 0.177, paired t test, n = 12). Right, same but for rheobase (P = 0.002, Wilcoxon test, n = 12). E–H, same as A–D but for pooled raw data of types 2 and 3 (type 2 + 3) (P = 0.820 Wilcoxon test and P < 0.001 paired t test, respectively, n = 10). ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
Article Snippet: In vitro pharmacology Drugs used for the study were as follows: GABAbR agonist baclofen, 10 μM (Sigma-Aldrich, St Louis, MO, USA), NMDA receptor antagonist d-2-amino-5-phosphonovaleric acid (APV), 50 μM (Tocris Bioscience, UK), AMPA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX), 20 μM (Tocris Bioscience, Bristol, UK), BK channel antagonist paxilline, 10 μM (Tocris Bioscience), GABAaR antagonist picrotoxin, 100 μM (Tocris Bioscience).
Techniques: Injection, Control, Comparison