Rostromedial tegmental nucleus
It is poorly differentiated from the rest of the ventral tegmental area (VTA) and possesses robust functional and structural links to the dopamine pathways.[1][2] Notably, both acute and chronic exposure to psychostimulants have been shown to induce FosB and ΔFosB expression in the RMTg;[1][2] no other drug type has been shown to induce these proteins in the RMTg.[1][2] The GABAergic neurons that project from the RMTg to the midbrain dopaminergic nuclei (i.e., the ventral tegmental area and substantia nigra pars compacta) express μ-opioid receptors.[1][2] Current evidence suggests that exogenous opiates (e.g., morphine and heroin) excite the dopamine pathways originating in the VTA by activating the μ-opioid receptors in neurons projecting from the RMTg;[1][2] opioid activation of these neurons leads to disinhibition of the GABAergic brake on dopamine networks.[1][2] Since RMTg projections to the VTA are the primary inhibitor of the dopaminergic pathways that are implicated in addiction (e.g., the mesolimbic pathway), the RMTg plays a significant role in the development of opiate addictions.