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. 2023 Jan 13;14:200. doi: 10.1038/s41467-023-35806-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a, b JAK (Ruxolitinib; 280 nM), ERK1/2 (PD98059; 20 μM) and STAT6 (AS1517499; 1 μM) inhibitors significantly abolish the IL-13 dependent CREB phosphorylation in rat cortical neurons (veh vs IL-13: p = 0.0002; IL-13 vs RUX: p = 0.0108; IL-13 vs PD: p = 0.0083; IL-13 vs AS: p = 0.0082). STAT3 inhibitor (Stattic; 20 μM) did not alter the IL-13 induced phosphorylation of CREB (IL-13 vs STAT: p = 0.9994). N = 3–4; n = veh: 268; IL-13: 275; Rux: 249; PD: 249; AS: 248; STAT: 199 neurons. c, d TrkB receptor antagonist (ANA-12; 10 μM), PKA inhibitor (H89; 10 μM) and CAMK-II inhibitor (KN93; 10 μM) significantly reduce the IL-13 induced CREB phosphorylation (veh vs IL-13: p = 0.0002; IL-13 vs ANA-12: p = 0.0012; IL-13 vs H89: p < 0.0001; IL-13 vs KN93: p < 0.0001). Both the CDK5 inhibitor (Roscovitine; 10 μM) and GSK-3 inhibitor (CHIR 98014; 10 μM) do not alter IL-13 induced CREB phosphorylation (IL-13 vs Rosco: p = 0.8861; IL-13 vs CHIR: p = 0.5020). N = 3; n = Veh: 282; IL-13: 301; ANA-12: 276; H89: 253; KN93: 262; Rosco: 264; CHIR: 251 neurons. e, f AMPA receptor antagonists (CNQX, NBQX; both 10 μM), NMDA receptor antagonist (MK-801; 10 μM) and calcium channel blocker (Mibefradil; 10 μM) significantly reduce the IL-13 induced CREB phosphorylation (veh vs IL-13: p = 0.0004; IL-13 vs CNQX: p = 0.0037; IL-13 vs NBQX: p = 0.0010; IL-13 vs MK801: p < 0.0001; IL-13 vs Mibef: p < 0.0001). N = 3; n = Veh: 190; IL-13: 160; CNQX: 197; NBQX: 198; MK801: 234; Mibef: 202 neurons. g, h Cell specific inhibition of the AMPAR using the YM90K-DART (100 nM) pharmacology tethered to a transmembranal HaloTag (HaloTag-TM) significantly decreases CREB phosphorylation 1 h post IL-13 treatment (50 ng/ml; p = 0.0157). N = 4; n = HT-/IL-13-: 440; HT+/IL-13-: 70; HT-/IL-13+: 322; HT+/IL-13+: 62 neurons. i, j Cell specific genetic mutagenesis of Grin1 using CRISPR-Cas9/BFP-Cre transfected cells significantly decreases CREB phosphorylation 1 h post IL-13 treatment (50 ng/ml: yellow arrows; p < 0.0001). N = 5; n = BFP-/IL-13-: 324; BFP+/IL-13-: 77; BFP-/IL-13+: 366; BFP+/IL-13+: 46 neurons. Vehicle (0.1% DMSO) was used as control in (a–f); (0.1% BSA) was used as control in (g–i). Scale bar: 20 μm. **: p < 0.01; ***: p < 0.001; ****: p < 0.0001. b, d, f, h, j One-way ANOVA with Sidak’s multiple comparison. Source data are provided as a Source Data file.