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Updated: Jan 19, 2026

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
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.
Abstract:
Growing evidence shows that autophagy is deficient in neurodegenerative and psychiatric diseases, and that its induction may have beneficial effects in these conditions. However, as autophagy shares signaling pathways with cell death and interferes with protein synthesis, prolonged use of autophagy inducers available nowadays is considered unwise. The search for novel autophagy inducers indicates that DRD2 (dopamine receptor 2)-DRD3 ligands may also activate autophagy, though critical aspects of the action mechanisms and effects of dopamine ligands on autophagy are still unknown. In order to shed light on this issue, DRD2- and DRD3-overexpressing cells and drd2 KO, drd3 KO and wild-type mice were treated with the DRD2-DRD3 agonist pramipexole. The results revealed that pramipexole induces autophagy through MTOR inhibition and a DRD3-dependent but DRD2-independent mechanism. DRD3 activated AMPK followed by inhibitory phosphorylation of RPTOR, MTORC1 and RPS6KB1 inhibition and ULK1 activation. Interestingly, despite RPS6KB1 inhibition, the activity of RPS6 was maintained through activation of the MAPK1/3-RPS6KA pathway, and the activity of MTORC1 kinase target EIF4EBP1 along with protein synthesis and cell viability, were also preserved. This pattern of autophagy through MTORC1 inhibition without suppression of protein synthesis, contrasts with that of direct allosteric and catalytic MTOR inhibitors and opens up new opportunities for G protein-coupled receptor ligands as autophagy inducers in the treatment of neurodegenerative and psychiatric diseases.
Abbreviations:
AKT/Protein kinase B: thymoma viral proto-oncogene 1; AMPK: AMP-activated protein kinase; BECN1: beclin 1; EGFP: enhanced green fluorescent protein; EIF4EBP1/4E-BP1: eukaryotic translation initiation factor 4E binding protein 1; GPCR; G protein-coupled receptor; GFP: green fluorescent protein; HEK: human embryonic kidney; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAP2K/MEK: mitogen-activated protein kinase kinase; MAPK1/ERK2: mitogen-activated protein kinase 1; MAPK3/ERK1: mitogen-activated protein kinase 3; MDA: malonildialdehyde; MTOR: mechanistic target of rapamycin kinase; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; PPX: pramipexole; RPTOR/raptor: regulatory associated protein of MTOR, complex 1; RPS6: ribosomal protein S6; RPS6KA/p90S6K: ribosomal protein S6 kinase A; RPS6KB1/p70S6K: ribosomal protein S6 kinase B1; SQSTM1/p62: sequestosome 1; ULK1: unc-51 like autophagy activating kinase 1; WT: wild type.
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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