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2 3 dihydroxy 6 nitro 7 sulfamoyl benzo f quinoxaline 2 3 dione nbqx

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2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione(NBQX) is a selective and potent antagonist of AMPA and kainate receptors. It functions by inhibiting the activity of these glutamate-gated ion channels.

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4 protocols using 2 3 dihydroxy 6 nitro 7 sulfamoyl benzo f quinoxaline 2 3 dione nbqx

1

Recombinant BDNF and β-NGF Protocol

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Human recombinant BDNF and human recombinant β-NGF were
purchased from Millipore, K252a and d-2-amino-5-phosphonovalerate (d-AP5) and
2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione
(NBQX) were from Tocris, human-IgG was from Sigma, and
1′-naphthylmethyl-4-amino-1-tert-butyl-3-(p-methylphenyl)pyrazolo[3,4-d]
pyrimidine (1NMPP1) was from Santa Cruz and Shanghai Institute of Materia
Medica, Chinese Academy of Sciences. TrkB-Ig was a gift from Regeneron and the
tat-CN21 peptide (YGRKKRRQRRRKRPPKLGQIGRSKRVVIEDDR) was synthesized by
GenScript.
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2

Modulation of Septal-Hippocampal Theta Rhythms

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The following drugs were administered intracerebrally in the study: (a) muscimol hydrobromide (0.5 μl of 2 μg/μl solution; Sigma, USA), muscimol being a GABA mimetic28 (link), (b) (2 R)-amino-5-phosphonopentanoate (AP5; 0.5 μl of 5 μg/μl solution; Sigma, USA) which is an antagonist at the glutamate NMDA receptors68 (link),89 (link),90 (link), (c) 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBQX; 0.5 μl of 10 μg/μl, 20 μg/μl or 40 μg/μl solution; Tocris, USA) which is an antagonist at glutamate AMPA receptor39 (link),92 (link), and (d) lidocaine hydrochloride (0.5 μl/site of 4% w/v; Sigma, USA), a local anesthetic50 (link). The drugs were prepared in 0.5% Alcian blue dye in saline (Sigma, USA) which also acted as vehicle in control experiments. The drugs, (a) through (c), were used in experiments involving microinjection into the MS region. Intraseptal microinjections were made at one given site only, while, in comparison, lidocaine was microinjected bilaterally into the RVM.
Functionally, intraseptal microinjection of the fore-mentioned drugs at the selected concentration attenuates theta rhythmic septo- hippocampal activation28 (link),68 (link),89 (link)–91 (link). The highest concentration of NBQX used in this study is also known to strongly attenuate afferent stimulation-evoked putative AMPA current in medial septal neurons39 (link).
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3

Optogenetic Manipulation and Pharmacological Modulation

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Viral vectors (adeno-associated virus [AAV]-channelrhodopsin 2 [ChR2]-tdTomato, AAV-Chronos-green fluorescent protein [GFP], and AAV-Chrimson-tdTomato) were purchased from the University of North Carolina (Vector Core Facility). Ro 25–6981, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBQX), and (2R)-amino-5-phosphonovaleric acid; (2R)-amino-5-phosphonopentanoate (APV) were obtained from Tocris. All other reagents were purchased from Sigma.
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4

Pharmacological Modulation of Neuronal Activity

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For pharmacological experiments, reagents were dissolved in ACSF and applied on the cranial window from 30 min preceding imaging. Tetrodotoxin (TTX, 2 μM, Tocris) was used to block sodium channel. DL-2-amino-5-phosphonovaleric acid (AP-5, 50 μM, Tocris) and 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline-2,3-dione (NBQX, 20 μM, Tocris) were used to block NMDA-type and AMPA-type ionotropic glutamate receptors, respectively. Prazosin hydrochloride (200 μM, Sigma–Aldrich) was used to block alpha-1 adrenergic receptors (A1ARs).
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