Given that the aforementioned CMS-induced regulation of CB1 was studied using either western immunoblotting (Hill et al., 2005; Reich et al, 2009) or competitive binding assays (Hill et al, 2005; Hill et al., 2008a), it is unknown whether these differences are represented in the general CB1 population or in a particular sub-population. Moreover, it remains unclear how these stress-induced changes affect synaptic physiology in the hippocampus. For example, in the CA1 region of the rodent hippocampus, CB1 resides primarily on the nerve terminals of cholecystokinin (CCK)-containing interneurons (Freund, 2003) and at the glutamatergic synapse between the CA3 Schaffer collateral/commissural terminals and CA1 pyramidal cells (Domenici et al., 2006; Kawamura et al., 2006). Although, compared to the CCK-GABA cells, the glutamatergic-CA3 cells contain a much lower density of CB1 (Domencini et al., 2006; Kawamura et al., 2006). Thus, the primary purpose of this study is to assess if CMS differentially affects CB1-mediated glutamatergic and GABAergic neurotransmission.
