The finding that more significant abnormalities were identified in the dorsal striatum in adulthood is consistent with our previous report of impairment in dorsal (but not ventral) striatal long-term depression (LTD) as a functional neurophysiological change in synaptic plasticity in adult male offspring with parental THC exposure (Szutorisz et al., 2014). The mechanistic nature of the observed increased LTD remains to be explored in detail neurophysiologically. For example, which subtype of glutamate receptors are responsible for the observed effects and whether the synaptic plasticity is mediated by the endocannabinoid system needs to be investigated. The fact that parental THC exposure caused a highly significant strengthening of mRNA expression patterns between the Cnr1 gene (which encodes the CB1 receptor) and various glutamate receptor subunit genes (especially Grin2A), as well as Dlg4 and Dlgap3, is intriguing and suggests indeed an endocannabinoid link mechanistically that will be examined in subsequent neurophysiological studies.
