recordings from adolescent male animals exposed to CMS, we hypothesized that CMS-downregulation of CB1 would impair function on both glutamatergic and GABAergic synapses. However, we observed that CMS does not affect glutamate-CB1 function directly but does increase glutamatergic neurotransmission through a sensitized GABA-CB1 function. This enhanced CB1 function on GABAergic neurotransmission also facilitates LTP induction to weak theta-burst stimulation and shifts the dependency of LTP inhibition by CB1 agonists from glutamatergic to GABAergic neurotransmission.
