The P2X7 receptor is an adenosine triphosphate (ATP)-gated ion channel expressed in different cell types of the brain. Polymorphisms in the P2RX7 gene have repeatedly been associated with psychiatric disorders including major depression. Depression is a stress-related disorder in which a dysregulation of the immune system has attracted increasing attention as a potential disease mechanism. The well-documented role of P2X7 in inflammatory conditions advocates its involvement in immune system dysregulation and depression genesis. However, understanding its exact role requires further research using appropriate animal models. Unfortunately, some of the most widely used P2X7 knockout mouse models are limited in their utility by the continuous expression of certain P2rx7 splice variants or even activation of de novo transcripts. To overcome this limitation, we generated a novel constitutive and complete P2X7 KO mouse line. These KO mice lack all known murine splice variants and protein expression resulting in a loss-of-function as confirmed by calcium imaging and by the inability of P2X7-deficient peritoneal macrophages to mount an appropriate interleukin (IL)-1β response. Comprehensive characterization using a battery of tests assessing locomotion, anxiety- and depression-related as well as social behaviour revealed differences in locomotor and exploratory behaviours. P2X7 KO mice showed slightly increased locomotor activity and reduced anxiety-related behaviour at baseline. Under conditions of chronic stress exposure, genotype-dependent differences largely dissolved while P2X7 deficiency promoted enhanced stress resilience with regard to social behaviour. Taken together, our findings add further evidence for an involvement of the P2X7 in shaping different behavioural responses and their modulation by stressful environments. This novel loss-of-function model will contribute to a better understanding of P2X7 in stress-associated behaviours in basic and translational neuropsychiatric research.
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http://dx.doi.org/10.1007/s11302-025-10074-x | DOI Listing |
Purinergic Signal
March 2025
Université Côte dAzur, CNRS, INSERM, IRCAN, Nice, France.
Over the past few years, transcriptomics has emerged as a pillar for modern scientific research, enabling the comprehensive profiling of gene expression. The availability of large-scale public datasets, such as NCBI Gene Expression Omnibus, International Cancer Genome Consortium, and The Cancer Genome Atlas, has significantly boosted many scientific discoveries. However, to analyze and interpret these vast datasets, sophisticated bioinformatic tools are often necessary.
View Article and Find Full Text PDFAdv Sci (Weinh)
March 2025
Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
The dysregulation of the M1/M2 macrophage balance plays a pivotal role in autoimmune diseases. However, the interplay between microRNAs (miRNAs) and N6-methyladenosine (m6A) modulation in regulating this balance remains poorly understood. Here, a significant reduction in miR-31-5p levels is observed in the lacrimal glands of rabbit autoimmune dacryoadenitis and the peripheral blood mononuclear cells (PBMCs) of Sjögren's syndrome (SS) dry eye patients.
View Article and Find Full Text PDFSci Rep
March 2025
Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chuncheon, 24252, Korea.
P2X7 receptor (P2X7R) augments lipopolysaccharide (LPS)-toll-like receptor 4 (TLR4)-mediated neuroinflammation. These roles of P2X7R in neuroinflammation are relevant to nitrosative stress through nuclear factor-κB (NF-κB)-inducible nitric oxide synthase (iNOS) pathway, while the underlying mechanisms are largely unknown. In the present study, we investigated whether protein disulfide isomerase (PDI) is involved in the integration of TLR4-P2X7R functions in response to LPS in vivo.
View Article and Find Full Text PDFMol Cell Neurosci
March 2025
Department of Anatomy and Neurobiology, Institute of Epilepsy Research, College of Medicine, Hallym University, Chuncheon 24252, South Korea.
Glutathione (GSH) and heat shock protein 25 (HSP25) reciprocally regulate each other, which maintain redox homeostasis. Since P2X7 receptor (P2X7R) regulates GSH biosynthesis and HSP25 induction, the present study was conducted to explore the role of P2X7R in the reciprocal regulation between HSP25 and GSH in response to kainic acid (KA)-induced nitrosative stress and the related signal pathways, which are largely unknown. The present data demonstrate that P2X7R deletion attenuated KA-induced reductions in total GSH level and nuclear factor-erythroid 2-related factor 2 (Nrf2) intensity/nuclear translocation in astrocytes.
View Article and Find Full Text PDFJ Neuroinflammation
March 2025
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen University, Guangzhou, 510060, China.
Background: Impairment of the inner blood-retinal barrier (iBRB) leads to various blinding diseases including diabetic retinopathy (DR). The cGAS-STING pathway has emerged as a driving force of cardiovascular destruction, but its impact on the neurovascular system is unclear. Here, we show that cGAMP, the endogenous STING agonist, causes iBRB breakdown and retinal degeneration thorough P2RX7-mediated transport into microglia.
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