cnqx  (Alomone Labs)

Journal: Cells

Article Title: Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream H2S/Cav3.2 Signaling in Mice

doi: 10.3390/cells9081748

Figure Lengend Snippet: Effect of T-type Ca 2+ channel blockers and genetic deletion of Ca v 3.2 on CPA-induced bladder pain-like nociceptive behavior ( A , D , G , J ), referred hyperalgesia ( B , E , H , K ) and bladder swelling ( C , F , I , L ) in mice. ( A – F ) In ddY mice, 6-prenylnaringenin (6-PNG), a hop-derived T-type Ca 2+ channel blocker, or KTt-45, a derivative of 6-PNG, at 10 and 30 mg/kg was administered i.p. 3 h 15 min after i.p. CPA at 400 mg/kg. ( G – I ) In C57BL/6 mice, TTA-A2 at 1 mg/kg was administered i.p. 3 h after the CPA treatment. ( J – L ) CPA at 400 mg/kg was administered i.p. to wild-type (WT) and Ca v 3.2-knockout mice (KO) of a C57BL/6J background. Nociceptive behaviors were counted for 30 min starting 3.5 h after CPA treatment, followed immediately by evaluation of referred hyperalgesia/allodynia and then measurement of wet tissue weight of the excised bladder. V, vehicle. Data show the mean with S.E.M. for 6–8 (A–C), 5 (D–F), 5–6 (G–I) or 6 (J–L) mice. * p

Article Snippet: TTA-A2 was obtained from Alomone Labs. (Jerusalem, Israel), and A438079, 5-BDBD and AZ 10606120 were from Tocris Bioscience (Bristol, UK). (2R/S)-6-Prenylnaringenin (6-PNG) and KTt-45 [6-(3-ethylpent-2-enyl)-5,7-dihydroxy-2-(2-hydroxyphenyl)chroman-4-one] were synthesized in-house, as reported previously [ ].

Techniques: Mouse Assay, Derivative Assay, Knock-Out

Journal: PLoS ONE

Article Title: T-type calcium channel enhancer SAK3 promotes dopamine and serotonin releases in the hippocampus in naive and amyloid precursor protein knock-in mice

doi: 10.1371/journal.pone.0206986

Figure Lengend Snippet: SAK3 may promote DA and 5-HT release via stimulating T-type calcium channels and nAChRs. (A) NNC 55–0396 (1 μM), TTA-A2 (1 μM), DhβE (100 μM), or MLA (1 nM) treatment through the microdialysis probe inhibited DA release following SAK3 (0.5 mg/kg, p.o.) administration in the CA1 region (n = 4–10 per group). Error bars represent the SEM. (B) AUC of DA levels at time point from 0 to 60 min were calculated. *p

Article Snippet: While T-type calcium channel inhibitor NNC 55–0396 (1 μM) significantly inhibited SAK3-promoted hippocampal DA and 5-HT releases, the same dose of TTA-A2 (1 μM) failed to inhibit SAK3 effect completely.

Techniques:

Journal: Molecular Brain

Article Title: Presynaptic muscarinic acetylcholine autoreceptors (M1, M2 and M4 subtypes), adenosine receptors (A1 and A2A) and tropomyosin-related kinase B receptor (TrkB) modulate the developmental synapse elimination process at the neuromuscular junction

doi: 10.1186/s13041-016-0248-9

Figure Lengend Snippet: Changes in polyneuronal innervation of the NMJ after stimulation and inhibition of the mAChR. The figure shows the percentage of singly-, dually- and triply- (or more) innervated NMJs in the untreated YFP control mice (exposed to PBS applications) and after 2 (P7 in a ), 4 (P9, in b ) and in some cases 10 (P15, in c ) applications (one application every day after P5) of the mAChR agonist (ago.) oxotremorine (OXO) and such antagonists (ant.) as atropine (AT), pirenzepine (PIR), methoctramine (MET) and muscarinic toxin 3 (MT3). Fisher’s test: * p

Article Snippet: Selective M1 , M2 and M4 mAChR antagonists The stock solutions were pirenzepine dihydrochloride (PIR; 1071, Tocris Bioscience) 10 mM; methoctramine (MET; M105, Sigma – Aldrich, St. Louis, MO) 1 mM; muscarinic toxin 3 (MT-3; M-140, Alomone Labs) 50 μM.

Techniques: Inhibition, Mouse Assay