PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
May 3, 20260 citations

Purinergic signaling: a novel therapeutic target in depression.

View Full Paper
QCQianqian CuiYLYunxiao LiSGShuangqi Gao

Key Points

  • To review the role of purinergic signaling in the pathogenesis of major depressive disorder and its therapeutic potential.
  • Systematic review of literature on purinergic signaling and depression sourced from PubMed.
  • Focus on molecular mechanisms involving ATP, adenosine, astrocytes, neuronal plasticity, and microglia.
  • Discussion of limitations and controversies in current research.
  • Purinergic signaling influences neuronal plasticity and the function of astrocytes and microglia.
  • Emerging evidence supports the therapeutic potential of targeting purinergic pathways in treating depression.
  • Continued exploration is required due to controversies and limitations in available research.

Abstract

Major depressive disorder, as a common neuropsychiatric disorder, has a complex pathogenesis that has not yet been fully elucidated, posing significant challenges to clinical treatment. In recent years, the role of the purinergic signaling system in the pathophysiological processes of depression has garnered increasing attention. The purinergic signaling primarily involves extracellular purine compounds such as ATP and adenosine, which act as transmitters by binding to their corresponding purine receptors (P1 and P2). Purinergic signaling can participate in depression by affecting the function of astrocytes, neuronal plasticity, and the activity of microglia. This paper systematically reviews the latest research advancements in purinergic signaling related to depression by searching for articles on the pubmed using the keywords "purinergic" OR "ATP" OR "adenosine" and "depression". It focuses on the molecular mechanisms of action and discusses the limitations and controversial issues present in current research, aiming to provide new theoretical foundations and treatment strategies for the precise treatment of depression.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Cui et al. (2026) studied this question.

synapsesocial.com/papers/69f6e5618071d4f1bdfc614dhttps://doi.org/10.1080/00207454.2026.2666245
Ask AI
Helpful
Bookmark
Share
View Full Paper

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Gut microbiota dysbiosis contributes to depression-like behaviors via hippocampal NLRP3-mediated neuroinflammation in a postpartum depression mouse model2024 · 77 citations
  2. 2Impaired long‐term depression in P2X3 deficient mice is not associated with a spatial learning deficit2006 · 29 citations
  3. 3Guanosine controls inflammatory pathways to afford neuroprotection of hippocampal slices under oxygen and glucose deprivation conditions2013 · 101 citations
  4. 4Rat brain guanosine binding site2003 · 70 citations
  5. 5Inflammation and Blood-Brain Barrier in Depression: Interaction ofCLDN5andIL6Gene Variants in Stress-Induced Depression2022 · 34 citations