Rostromedial tegmental nucleus
The rostromedial tegmental nucleus (RMTg), or tail of the ventral tegmental area (tVTA), is a GABAergic nucleus which functions as a "master brake" for the midbrain dopamine system.[1][2] 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.[2]
Inputs
The RMTg receives incoming projections from the following structures:[2]
- Medial prefrontal cortex
- Cingulate cortex
- Preoptic area
- Lateral hypothalamus
- Lateral habenula
- Superior colliculus
- Periaqueductal gray
- Dorsal raphe
- Laterodorsal tegmental nucleus
- Substantia nigra
- Nucleus accumbens
- Pontine tegmentum
- Ventral pallidum
Outputs
GABA projections from the RMTg include:[2]
- RMTg → Raphe nuclei
- RMTg → Preoptic area
- RMTg → Lateral hypothalamus
- RMTg → Substantia nigra
- RMTg → VTA
- RMTg → Periaqueductal gray
- RMTg → Pontine tegmentum
Clinical significance
The RMTg plays a "crucial role" in the regulation of CNS dopaminergic activity by endogenous opioids and opiate drugs.[1][2] The GABAergic neurons that project from the RMTg to midbrain dopamine systems express μ-opioid receptors.[1][2] Current models of this system suggest that exogenous opiates (e.g., morphine) excite 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 VTA-originating addiction pathways (most notably the mesolimbic pathway), the RMTg plays a dominant role in the development of opiate addictions.[1][2][3]
Psychostimulants have been shown to increase expression of the FosB and ΔFosB in the RMTg;[1][2] the involvement in stimulant addiction and effects of ΔFosB expression in the RMTg have not yet been identified.
