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We thus performed OGTTs on Glp1r OB-hM3Dq WD mice after chemogenetic activation of OB Glp1r -expressing neurons with concurrent blockade of GABA A R in the PVN, using a local injection of the GABA A R antagonist bicuculline (Fig

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In tolerance assay, at 42 h after the end of conditioning regimen, shorter preconvulsive latencies than in healthy (non-diazepam conditioned) mice following isoniazid (800 mg/kg i.p.) (as hallmark of tolerance) were observed if diazepam (5.0 mg/kg i.p.) was again given acutely to mice previously conditioned with diazepam alone (use of picrotoxin 3.0 mg/kg i.p., as convulsant, with acute application of diazepam in previously diazepam conditioned mice did not lead to tolerance hallmark)