Building on the GO analysis, we further explored the relationship of DMR-associated genes and additional gene sets of interest associated with biological processes that we would expect to be altered in this model. Specifically, it is well established and is in line with our previous observations that glutamatergic-related genes such as glutamate receptors (GluRs) play important roles in mediating synaptic plasticity and transmission, with impacts on behavior including those involved in addiction (Szutorisz et al, 2014). For example, we have previously shown that F1 adult rats with parental THC exposure show electrophysiological impairments related to dysregulation of synaptic plasticity (Szutorisz et al, 2014). Consistent with these phenotypes, many DMRs overlapped genes encoding regulators of synaptic plasticity, including GluRs and kainite receptors (Grin2a, Grik3, and Grik5), G-protein-coupled receptors (GPCRs; Gpr39, Gpr157, and Gpr158), pre- and postsynaptic ion channels (Cacna1a, Kcna5, Kcnma1, Kcnq2, Kcnh1, Kcnn1, Kcnm, Kcnj10, Kcnn4, Kcnq1, Hcn3, Scn5a, and Scn8a) and scaffolding proteins (Table 2). Thus, to more directly explore the relationship between THC-induced DNA methylation changes and genes involved in the glutamatergic system and synaptic transmission, we used
