DRD3 (dopamine receptor D3) but not DRD2 activates autophagy through MTORC1 inhibition preserving protein synthesis

Pedro Barroso-Chinea1,2, Diego Luis-Ravelo1,2, Felipe Fumagallo-Reading1,2

  • 1Departamento de Ciencias Médicas Básicas, Facultad de Medicina, Universidad de La Laguna , Tenerife, Spain.

Autophagy
|September 21, 2019
PubMed

Insights

Pramipexole induces autophagy via a dopamine D3 receptor (DRD3) mechanism, inhibiting MTOR without suppressing protein synthesis. This offers a novel therapeutic strategy for neurodegenerative and psychiatric diseases.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Autophagy is deficient in neurodegenerative and psychiatric diseases, and its induction shows therapeutic potential.
  • Current autophagy inducers have limitations due to interference with cell death and protein synthesis pathways.
  • Dopamine receptor ligands are being investigated as novel autophagy inducers, but their mechanisms are unclear.

Purpose of the Study:

  • To investigate the mechanism by which pramipexole, a DRD2-DRD3 agonist, modulates autophagy.
  • To determine the specific dopamine receptor (DRD2 or DRD3) involved in pramipexole-induced autophagy.
  • To elucidate the downstream signaling pathways affected by pramipexole in relation to autophagy and protein synthesis.

Main Methods:

  • Utilized DRD2- and DRD3-overexpressing cells, as well as drd2 knockout (KO), drd3 KO, and wild-type (WT) mice.
  • Treated cells and mice with pramipexole (PPX).
  • Analyzed autophagy induction, MTOR signaling, AMPK activation, protein synthesis, and cell viability.

Main Results:

  • Pramipexole induced autophagy through a DRD3-dependent, DRD2-independent mechanism involving MTOR inhibition.
  • DRD3 activation led to AMPK activation, RPTOR phosphorylation, MTORC1 and RPS6KB1 inhibition, and ULK1 activation.
  • Protein synthesis and cell viability were preserved due to compensatory activation of the MAPK1/3-RPS6KA pathway, maintaining RPS6 activity and EIF4EBP1 function.

Conclusions:

  • Pramipexole activates autophagy via a unique MTOR inhibition pathway that preserves protein synthesis, unlike conventional MTOR inhibitors.
  • This mechanism highlights the potential of G protein-coupled receptor (GPCR) ligands, specifically DRD3 agonists, as novel therapeutic agents for neurodegenerative and psychiatric disorders.
  • The findings open new avenues for developing safer and more effective autophagy-inducing drugs by targeting specific receptor pathways.

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