Qx 314 chloride

D-AP5 (D-(-)−2-Amino-5-phosphopentanoic acid), SR 95531 (2–3-Carboxyprobyl)−3-amino-6(4-methoxyphenyl pyridazinium bromide), and QX-314 chloride were purchased from Abcam, Cambridge, UK. NBQX (2,3-Dioxo-6nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide) was purchased from Tocris Bioscience, Bristol, UK. Alexa Fluor 488 and 594 were purchased from Life Technologies, Carlsbad, California, USA. Mefloquine hydrochloride and DMSO (Dimethyl sulfoxide) were bought from Sigma-Aldrich, St Louis, Missouri, USA.

All recordings were made in the presence of picrotoxin (PTX; 100 µM, Abcam) to block GABA_A receptors, except for dual pathway experiments where gabazine (GBZ; 10 µM, Abcam) was used instead to reduce the external concentration of DMSO. NMDA receptor responses were blocked with R-CPP (5 µM, Abcam) in all recordings. In experiments involving dual-pathway stimulation, blockers of L-type Ca²⁺channels (nifedipine; 10 µM, Tocris), T-type Ca²⁺ channels (TTA-P2; 5 µM, Alomone Labs), and CB1 receptors (AM251; 1 µM, Cayman Chemical Company) were applied along with R-CPP. AMPARs were blocked using either NBQX (10 µm, Abcam) or NASPM trihydrochloride (50–100 µM, Tocris). GABA_B receptors were activated using the agonist (R)-baclofen (3 µM, Tocris) and antagonized using CGP55845 hydrochloride (1 µM, Abcam). mGluR1 receptors were blocked with CPCCOEt (100 µM, Abcam). All drugs were applied via the external recording solution, except for QX-314 chloride (5 mM, Abcam), which was used in all experiments to block voltage-dependent Na⁺ channels and was added to the internal solution.