Journal: Advanced Science

Article Title: Stage‐Specific H3K14 and H3K23 Succinylation Orchestrates Insect Metamorphosis and Oogenesis

doi: 10.1002/advs.75624

Figure Lengend Snippet: Regulation of suc‐H3 K14 and suc‐H3 K23 by the GPCR‐RTK‐PLC‐PKC cascade. (A) Effect of GPCR (Suramin), RTK (SU6668/genistein), PLC (U73122), CaMKII (KN‐93), and PKC (CCL) inhibitors on JH‐induced suc‐H3 K14 in the fourth instar nymphs. (B) Effect of Ca 2+ channel blockers (felodipine, L‐type; flunarizine, T‐type; cav2.2, N‐type; ω‐Agatoxin TK, P/Q‐type; and SNX‐482, R‐type) on suc‐H3 K14 . (C) Knockdown efficiency of PKC isoforms in the fat body of fourth instar nymphs. ** , p < 0.01; n = 3. (D) Effect of PKC isoform knockdown on suc‐H3 K14 . (E, F) Effect of GPCR, RTK, PLC, CaMKII, and PKC inhibitors ( E ) and Ca 2+ channel blockers ( F ) on JH‐induced suc‐H3 K23 in the adult females. (G) Knockdown efficiency of PKC isoforms in the adult females. ** , p < 0.01; n = 3). (H) Effect of PKC isoform knockdown on suc‐H3 K23 in the adult females.

Article Snippet: In pharmacological experiments, the early fourth instar nymphs and previtellogenic adults of L. migratoria were injected with suramin (KKL MED; 30 μg, 150 μg), SU6668 (Selleck; 0.6 μg, 3 μg), genistein (MCE; 1.2 μg, 6 μg), U73122 (MCE; 2 μg, 10 μg), KN‐93 (MCE; 0.5 μg, 10 μg), CCL (Selleck; 1 μg, 5 μg), flunarizine (Selleck; 10 μg, 50 μg), Felodipine (TOPSCIENCE; 1 μg, 5 μg), Cav2.2 blocker 1 (TOPSCIENCE; 2 μg, 10 μg), ω‐Agatoxin TK (MCE; 0.25 μg,1 μg) and SNX‐482 (MCE; 0.25 μg, 1 μg), followed by JH or DMSO treatment for 30 min.

Techniques: Knockdown

Journal: Molecular Psychiatry

Article Title: Dopaminergic tone inhibits spontaneous glutamate release and augments homeostatic synaptic plasticity

doi: 10.1038/s41380-025-03374-6

Figure Lengend Snippet: A Graphical abstract illustrating working hypothesis on actions of dopamine tone on spontaneous glutamate release. B Graphical depiction showing experimental paradigm for rotundine (200 nM or 10 μM) or levosulpride perfusions. C Representative mEPSC traces for rotundine (200 nM or 10 μM) or levosulpride perfusions. [Treatment duration: acute perfusion (seconds to minutes)]. D Amplitudes of mEPSC events at baseline and after rotundine (200 nM or 10 μM) or levosulpride perfusions. (Baseline, n = 7, Mean = 15.42 ± 1.36 S.E.M.; 200 nM Rotundine perfusion, n = 7, Mean = 16.46 ± 2.05 S.E.M.; Baseline, n = 13, Mean = 14.34 ± 0.97 S.E.M.; 10 μM Rotundine Perfusion, n = 13, Mean = 14.45 ± 2.33 S.E.M.; Baseline, n = 10, Mean = 16.74 ± 1.61 S.E.M.; 10 μM Levosulpride Perfusion, n = 10, Mean = 16.04 ± 2.30 S.E.M.). E Frequency of mEPSC events at baseline and after rotundine (200 nM or 10 μM) or levosulpride perfusions. (Baseline, n = 7, Mean = 5.72 ± 1.37 S.E.M.; 200 nM Rotundine perfusion, n = 7, Mean = 6.48 ± 1.22 S.E.M.; Baseline, n = 13, Mean = 4.15 ± 1.00 S.E.M.; 10 μM Rotundine Perfusion, n = 13, Mean = 6.48 ± 1.51 S.E.M.; Baseline, n = 10, Mean = 4.23 ± 1.51 S.E.M.; 10 μM Levosulpride Perfusion, n = 10, Mean = 5.96 ± 1.40 S.E.M.). F Graphical abstract illustrating Agatoxin, conotoxin and SNX482 (VGCC cocktail) blocking presynaptic VGCCs. G Graphical depiction showing experimental paradigm for rotundine (200 nM or 10 μM) or levosulpride perfusions in the presence of VGCC cocktail [Treatment duration: acute perfusion (seconds to minutes)]. H Representative mEPSC traces for rotundine (200 nM or 10 μM) or levosulpride perfusions in the presence of VGCC cocktail. I Amplitudes of mEPSC events at baseline and after rotundine (200 nM or 10 μM) or levosulpride perfusions in the presence of VGCC cocktail. (Baseline, n = 8, Mean = 15.82 ± 1.32 S.E.M.; 200 nM Rotundine perfusion, n = 8, Mean = 14.99 ± 1.33 S.E.M.; Baseline, n = 11, Mean = 12.74 ± 0.95 S.E.M.; 10 μM Rotundine Perfusion, n = 11, Mean = 12.9 ± 0.68 S.E.M. ; Baseline, n = 16, Mean = 14.91 ± 1.08 S.E.M.; 10 μM Levosulpride Perfusion, n = 16, Mean = 14.86 ± 1.30 S.E.M.). J Frequency of mEPSC events at baseline and after rotundine (200 nM or 10 μM) or levosulpride perfusions in the presence of VGCC cocktail. (Baseline, n = 8, Mean = 5.19 ± 0.91 S.E.M.; 200 nM Rotundine perfusion, n = 8, Mean = 4.86 ± 0.60 S.E.M.; Baseline, n = 11, Mean = 3.38 ± 0.72 S.E.M.; 10 μM Rotundine Perfusion, n = 11, Mean = 3.21 ± 0.67 S.E.M. ; Baseline, n = 16, Mean = 4.95 ± 0.97 S.E.M.; 10 μM Levosulpride Perfusion, n = 16, Mean = 5.53 ± 1.33 S.E.M.). K Graphical depiction illustrating myristylation of ct-GRK2 to scavenge Gβγ subunit. L Graphical depiction showing experimental paradigm for Gβγ scavenging. M Representative mEPSC traces for pFUW (control) and myr ct-GRK2 groups at baseline and after levosulpride perfusion [Treatment duration: acute perfusion (seconds to minutes)]. N Amplitudes of mEPSC events in pFUW (control) and myr ct-GRK2 groups at baseline and after levosulpride perfusion. (Baseline-pFUW, n = 9, Mean = 14.66 ± 0.79 S.E.M.; Levosulpride Perfusion-pFUW, n = 9, Mean = 16.62 ± 1.87 S.E.M.; Baseline- myr ct-GRK2, n = 11, Mean = 18.28 ± 1.08 S.E.M.; Levosulpride Perfusion-myr ct-GRK2, n = 11, Mean = 19.3 ± 1.24 S.E.M.). O Frequency of mEPSC events in pFUW (control) and myr ct-GRK2 groups at baseline and after levosulpride perfusion. (Baseline-pFUW, n = 8, Mean = 2.43 ± 0.66 S.E.M.; Levosulpride Perfusion-pFUW, n = 8, Mean = 4.16 ± 1.01 S.E.M.; Baseline- myr ct-GRK2, n = 11, Mean = 4.60 ± 0.605 S.E.M.; Levosulpride Perfusion-myr ct-GRK2, n = 11, Mean = 4.88 ± 0.608 S.E.M.).

Article Snippet: VGCC inhibitor cocktail, including Cav2.1 blocker agatoxin, the Cav2.2 blocker conotoxin, and the Cav2.3 blocker SNX482, were obtained from Alamone Labs (Israel).

Techniques: Blocking Assay, Control