Rostromedial tegmental nucleus

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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]

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.

Notes

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References

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