Benidipine

Picrotoxin (50 μM), L-655 708 (11,12,13,13a-Tetrahydro-7-methoxy-9-oxo-9H-imidazo[1,5-a]pyrrolo[2,1 c][1,4]benzodiazepine-1-carboxylic acid, ethyl ester, 10 μM), SCS (Salicylidene salicylhydrazide, 1 μM), TPMPA ((1,2,5,6-Tetrahydropyridin-4-yl) methylphosphinic acid, 50 μM), etomidate (10 μM), allopregnanolone (100 nM), muscimol (5 μM), bumetanide (10 μM), nifedipine (10 μM), benidipine (10 μM), bay K 8644 (10 μM), bicuculline (50 μM), ATP (150 μM; all from Tocris Bioscience, Bristol, UK), SNAP ((S)-Nitroso-N-acetylpenicillamine, 50 μM), SC (semicarbazide 50 μM), GABA (5 μM), geneticin (10 μM; all from Sigma-Aldrich) and CPCPT (1-(3-Chlorophenethyl)−3-cyclopentylpyrimidine-2,4,6-(1H,3H,5H)-trione, 1 μM, Merck Millipore, Darmstadt, Germany) were used at the indicated concentrations, if not differently stated. All pharmacological treatments and live cell stainings were performed in CM at 37°C and 5% CO₂.

Lipopolysaccharide (LPS), 4-Diethylaminobenzaldehyde (DEAB; aldehyde dehydrogenase inhibitor), selegiline (MAO-B inhibitor), nifedipine (L-type VDCC inhibitor, all from Sigma-Aldrich), L-allylglycine (L-AG; GAD inhibitor), picrotoxin (GABA-A receptor inhibitor), bumetanide (NKCC1 inhibitor), benidipine (broad VDCC inhibitor, all from Tocris Bioscience), and 1-(3-Chlorophenethyl)-3-cyclopentylpyrimidine-2,4,6-(1H,3H,5H)-trione (CPCPT, CaV 1.3 inhibitor, Merck Millipore) were used at the indicated concentrations. Heat inactivation of T. gondii tachyzoites was performed at 56°C for 30 min. Supernatants were collected from microglia incubated with freshly egressed T. gondii tachyzoites (MOI 1, 24 h) and added at a final concentration of 1:1.