snx 482  (MedChemExpress)

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 Pain

Article Title: Characterization of excitatory synaptic transmission in the retrosplenial cortex of adult mice

doi: 10.1177/17448069251335500

Figure Lengend Snippet: N-type VGCCs in RSC excitatory synaptic transmission: (a) Samples of fEPSPs from all channels before and after bathing in ω-Ctx GVIA (1 μM). Channel 20 was stimulated with 9 μA (yellow flash). (b) Three channels with different levels of inhibition after applying ω-Ctx GVIA (1 μM) to a single slice for 30 min. Three different types of samples fEPSPs records acquired at the times indicated by the corresponding numbers are shown on the right side of the figure. (c) Average data for 10 activated channels in a slice. (d, e) Single and average fEPSPs slopes for 86 channels after ω-Ctx GVIA bathing. (f) Scale diagrams categorizing the degree of reduction of 86 channels after ω-Ctx GVIA TFA baths. Error bars represent SEM.

Article Snippet: N-type VGCCs blocker ω-Ctx GVIA, P/Q-type VGCCs blocker ω-Agatoxin IVA (ω-Aga IVA), L-type VGCCs blocker nimodipine and R-type VGCCs blocker SNX-482 were purchased from MedChemExpress (New Jersey, USA).

Techniques: Transmission Assay, Inhibition

Journal: Molecular Pain

Article Title: Characterization of excitatory synaptic transmission in the retrosplenial cortex of adult mice

doi: 10.1177/17448069251335500

Figure Lengend Snippet: Roles of other VGCCs in RSC synaptic transmission: (a) The figure shows the results after bathing in cadmium ( n = 5 slices/5 mice). The insets depict representative fEPSPs at specific time points indicated by the numerical indicators in the figure. (b) The graph shows the results after sequential bathing of ω-Ctx GVIA and Cd 2+ ( n = 5 slices/5 mice). The insets depict representative fEPSPs at specific time points indicated by the values in the graph. (c) Pooled data of 5 mice (105.1% ± 2.5% of baseline, n = 41 chs/5 slices/5 mice), showing the effect of applying ω-Aga IVA (1 μM) for 20 min. (d) Pooled data of 6 mice (103.4% ± 1.3% of baseline, n = 69 chs/6 slices/6 mice), showing the effect of applying SNX-482 (0.5 μM) for 20 min. (e) Pooled data of 11 mice (100.0% ± 1.7% of baseline, n = 106 chs/11 slices/11 mice), showing the effect of applying Ni 2+ (100 μM) for 20 min. (f) Pooled data of 16 mice (103.5% ± 0.9% of baseline, n = 106 chs/12 slices/12 mice), showing the effect of applying nimodipine (100 μM) for 30 min. All drugs infused had no effect on synaptic transmission in RSC. The horizontal bars indicate the period of drug application. Error bars represent SEM.

Article Snippet: N-type VGCCs blocker ω-Ctx GVIA, P/Q-type VGCCs blocker ω-Agatoxin IVA (ω-Aga IVA), L-type VGCCs blocker nimodipine and R-type VGCCs blocker SNX-482 were purchased from MedChemExpress (New Jersey, USA).

Techniques: Transmission Assay

Journal: Molecular Pain

Article Title: Characterization of excitatory synaptic transmission in the retrosplenial cortex of adult mice

doi: 10.1177/17448069251335500

Figure Lengend Snippet: A simplified model to explain N-type VGCCs-mediated excitatory synaptic transmission in RSC. Excitatory transmission in the RSC is mediated by glutamate receptors. Presynaptic N-VGCCs mainly contribute to neurotransmitter release in the RSC. Activation of presynaptic N-VGCCs induces calcium influx. Then, the presynaptic release of excitatory neurotransmitter glutamate is enhanced. NMDA receptors and AMPA receptors activated by glutamate leads to postsynaptic excitatory responses. Postsynaptic AMPA receptors play a dominating role in the synaptic transmission.

Article Snippet: N-type VGCCs blocker ω-Ctx GVIA, P/Q-type VGCCs blocker ω-Agatoxin IVA (ω-Aga IVA), L-type VGCCs blocker nimodipine and R-type VGCCs blocker SNX-482 were purchased from MedChemExpress (New Jersey, USA).

Techniques: Transmission Assay, Activation Assay