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purinergic signaling systems across comparative models of spinal cord injury

Neural Regeneration Research 2022年第3期17卷 2391-2398页

作者： Eva E.Stefanova Angela L.Scott Department of Pathology and Molecular Medicine McMaster UniversityHamiltonONCanada

Within the last several decades,the scientific community has made substantial progress in elucidating the complex pathophysiology underlying spinal cord injury.However,despite the many advances using conventional mammalian models,both cellular and axonal regeneration following spinal cord injury have remained out of reach.In this sense,turning to non-mammalian,regenerative species presents a unique opportunity to identify pro-regenerative cues and chara cterize a spinal cord microenvironment permissive to re-growth.Among the signaling pathways hypothesized to be dysregulated during spinal cord injury is the purinergic signaling system.In addition to its well-known role as energy currency in cells,ATP and its metabolites are small molecule neurotransmitte rs that mediate many diverse cellular processes within the central nervous system.While our unde rstanding of the roles of the purinergic system following spinal cord injury is limited,this signaling pathway has been implicated in all injury-induced secondary processes,including cellular death,inflammation,reactive gliosis,and neural regeneration.Given that the purinergic system is also evolutionarily conserved between mammalian and non-mammalian species,comparisons of these roles may provide important insights into conditions responsible for recovery success.Here,we compare the secondary processes between key model species and the influence of purinergic signaling in each context.As our understanding of this signaling system and pro-regenerative conditions continues to evolve,so does the potential for the development of novel therapeutic interventions for spinal cord injury.

关键词： cell death differenriation glia inflammation neurogenesis proliferation purinergic signaling reactive gliosis regeneration spinal cord injury teleost

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purinergic signaling and acupuncture analgesia

Purinergic signaling and acupuncture analgesia

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中国神经科学学会第十二届全国学术会议

作者： Hai-Yan YIN Yong TANG Chengdu University of Traditional Chinese Medicine

Acupuncture has been used in China from ancient times since more than 2,000 years ago. A variety of disorders can be treated effectively by inserting long, fine needles into specific acupuncture points（acupoints） on the skin of the patient’s body. Since acupuncture was proposed by National Institutes of Health（NIH） consensus in 1997 as a therapeutic intervention of complementary medicine, acupuncture efficacy has become more and more accepted in the Western world. Among acupuncture therapies, the acupuncture-induced analgesic effect has been used widely to alleviate diverse types of pain, particularly chronic pain. To date, acupuncture analgesia has drawn the attention of many investigators and become an important research subject of international interest around the world. Numerous studies have also demonstrated that acupuncture analgesia has physiological, anatomical and neurochemical basis despite that there is still an ongoing debate about the mechanism by which acupuncture alleviates pain. Since Professor Geoffrey Burnstock proposed that purinergic signalling, rather than a mystical subepidermal energy, may explain how acupuncture works in an article in Medical Hypotheses in 2009, the role of purinergic signalling in acupuncture research has gained much attention. So far, more scientists have got started to study the role of purinergic signalling in acupuncture-induced analgesia. In my talk, the work have been done by our group and other scientists will be summarized and where we are going and how we are going to get there in this amazing field will be described.

关键词： purinergic signaling Pain Acupuncture therapy

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Can glial cells save neurons in epilepsy?

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Neural Regeneration Research 2023年第7期18卷 1417-1422页

作者： Weida Shen Jelena BogdanovićPristov Paola Nobili Ljiljana Nikolić Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province School of MedicineZhejiang University City CollegeHangzhouZhejiang ProvinceChina Department of Life Sciences University of BelgradeInstitute for Multidisciplinary ResearchBelgradeSerbia Institute of Functional Genomics(IGF) University of MontpellierCNRSINSERMMontpellierFrance Department of Neurophysiology Institute for Biological Research Siniša StankovićNational Institute of Republic of SerbiaUniversity of BelgradeBelgradeSerbia

Epilepsy is a neurological disorder caused by the pathological hyper-synchronization of neuronal discharges.The fundamental research of epilepsy mechanisms and the targets of drug design options for its treatment have focused on neurons.However,approximately 30%of patients suffering from epilepsy show resistance to standard anti-epileptic chemotherapeutic agents while the symptoms of the remaining 70%of patients can be alleviated but not completely removed by the current medications.Thus,new strategies for the treatment of epilepsy are in urgent demand.Over the past decades,with the increase in knowledge on the role of glia in the genesis and development of epilepsy,glial cells are receiving renewed attention.In a normal brain,glial cells maintain neuronal health and in partnership with neurons regulate virtually every aspect of brain function.In epilepsy,however,the supportive roles of glial cells are compromised,and their interaction with neurons is altered,which disrupts brain function.In this review,we will focus on the role of glia-related processes in epileptogenesis and their contribution to abnormal neuronal activity,with the major focus on the dysfunction of astroglial potassium channels,water channels,gap junctions,glutamate transporters,purinergic signaling,synaptogenesis,on the roles of microglial inflammatory cytokines,microglia-astrocyte interactions in epilepsy,and on the oligodendroglial potassium channels and myelin abnormalities in the epileptic brain.These recent findings suggest that glia should be considered as the promising next-generation targets for designing anti-epileptic drugs that may improve epilepsy and drug-resistant epilepsy.

关键词： astrocyte cytokines glutamate ion channel microglia myelin neuron oligodendrocyte purinergic signaling seizures

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Integrating UHPLC-MS/MS quantitative analysis and exogenous purine supplementation to elucidate the antidepressant mechanism of Chaigui granules by regulating purine metabolism

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Journal of Pharmaceutical Analysis 2023年第12期13卷 1562-1576页

作者： Jiajun Chen Tian Li Dehua Huang Wenxia Gong Junsheng Tian Xiaoxia Gao Xuemei Qin Guanhua Du Yuzhi Zhou Modern Research Center for Traditional Chinese Medicine Shanxi UniversityTaiyuan030006China The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education Shanxi UniversityTaiyuan030006China The Key Laboratory of Effective Substances Research and Utilization in TCM of Shanxi Province Taiyuan030006China Institute of Materia Medica Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing100050China

Chaigui granules(CG)are a compound composed of six herbal medicines with significant antidepressant effects.However,the antidepressant mechanism of CG remains unclear.In the present study,we attempted to elucidate the antidepressant mechanism of CG by regulating purine metabolism and purinergic signaling.First,the regulatory effect of CG on purine metabolites in the prefrontal cortex(PFC)of chronic unpredictable mild stress(CUMS)rats was analyzed by ultra high-performance liquid chromatography tandem mass spectrometry(UHPLC-MS/MS)targeted quantitative analysis.Meanwhile,purinergic receptors(P2X7 receptor(P2X7R),A1 receptor(A1R)and A2A receptor(A2AR))and signaling pathways(nod-like receptor protein 3(NLRP3)inflammasome pathway and cyclic adenosine monophosphate(cAMP)-protein kinase A(PKA)pathway)associated with purine metabolism were analyzed by western blotting and enzyme-linked immunosorbent assay(ELISA).Besides,antidepressant mechanism of CG by modulating purine metabolites to activate purinergic receptors and related signaling pathways was dissected by exogenous supplementation of purine metabolites and antagonism of purinergic receptors in vitro.An in vivo study showed that the decrease in xanthine and the increase in four purine nucleosides were closely related to the antidepressant effects of CG.Additionally,purinergic receptors(P2X7R,A1R and A2AR)and related signaling pathways(NLRP3 inflammasome pathway and cAMP-PKA pathway)were also significantly regulated by CG.The results of exogenous supplementation of purine metabolites and antagonism of purinergic receptors showed that excessive accumulation of xanthine led to activation of the P2X7R-NLRP3 inflammasome pathway,and the reduction of adenosine and inosine inhibited the A1R-cAMP-PKA pathway,which was significantly ameliorated by CG.Overall,CG could promote neuroprotection and ultimately play an antidepressant role by inhibiting the xanthine-P2X7R-NLRP3 inflammasome pathway and activating the adenosine/inosine-A1R-cAMP-PKA pathway.

关键词： Chaigui granules Traditional Chinese medicine Antidepressant mechanism Purine metabolism purinergic signaling

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Study of the roles of caspase-3 and nuclear factor kappa B in myenteric neurons in a P2X7 receptor knockout mouse model of ulcerative colitis

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World Journal of Gastroenterology 2023年第22期29卷 3440-3468页

作者： Henrique Inhauser Riceti Magalhães Felipe Alexandre Machado Roberta Figueiroa Souza Marcos Antônio Ferreira Caetano Vanessa Ribeiro Figliuolo Robson Coutinho-Silva Patricia Castelucci Department of Surgery School of Veterinary Medicine and Animal SciencesUniversity of São PauloSão Paulo 05508-270Brazil Department of Anatomy University of São PauloSão Paulo 05508-000Brazil Biophysics Institute Carlos Chagas Filho Federal University of Rio de JaneiroRio de Janeiro 21941-902Brazil

BACKGROUND The literature indicates that the enteric nervous system is affected in inflammatory bowel diseases(IBDs)and that the P2X7 receptor triggers neuronal death.However,the mechanism by which enteric neurons are lost in IBDs is unknown.AIM To study the role of the caspase-3 and nuclear factor kappa B(NF-κB)pathways in myenteric neurons in a P2X7 receptor knockout(KO)mouse model of IBDs.METHODS Forty male wild-type(WT)C57BL/6 and P2X7 receptor KO mice were euthanized 24 h or 4 d after colitis induction by 2,4,6-trinitrobenzene sulfonic acid(colitis group).Mice in the sham groups were injected with vehicle.The mice were divided into eight groups(n=5):The WT sham 24 h and 4 d groups,the WT colitis 24 h and 4 d groups,the KO sham 24 h and 4 d groups,and the KO colitis 24 h and 4 d groups.The disease activity index(DAI)was analyzed,the distal colon was collected for immunohistochemistry analyses,and immunofluorescence was performed to identify neurons immunoreactive(ir)for calretinin,P2X7 receptor,cleaved caspase-3,total caspase-3,phospho-NF-κB,and total NF-κB.We analyzed the number of calretinin-ir and P2X7 receptor-ir neurons per ganglion,the neuronal profile area(μm^(2)),and corrected total cell fluorescence(CTCF).RESULTS Cells double labeled for calretinin and P2X7 receptor,cleaved caspase-3,total caspase-3,phospho-NF-κB,or total NF-κB were observed in the WT colitis 24 h and 4 d groups.The number of calretinin-ir neurons per ganglion was decreased in the WT colitis 24 h and 4 d groups compared to the WT sham 24 h and 4 d groups,respectively(2.10±0.13 vs 3.33±0.17,P<0.001;2.92±0.12 vs 3.70±0.11,P<0.05),but was not significantly different between the KO groups.The calretinin-ir neuronal profile area was increased in the WT colitis 24 h group compared to the WT sham 24 h group(312.60±7.85 vs 278.41±6.65,P<0.05),and the nuclear profile area was decreased in the WT colitis 4 d group compared to the WT sham 4 d group(104.63±2.49 vs 117.41±1.14,P<0.01).The number of P2X7 receptor-ir neurons per ganglion was decrea

关键词： Cell death Enteric nervous system Gastroenterology Inflammatory bowel diseases P2X7 receptor purinergic signaling

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Implication of Neuronal Versus Microglial P2X4 Receptors in Central Nervous System Disorders

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Neuroscience Bulletin 2020年第11期36卷 1327-1343页

作者： Alexia Duveau Eleonore Bertin Eric Boue-Grabot Universite de Bordeaux Institut des Maladies NeurodegenerativesUMR 529333000 BordeauxFrance CNRS Institut des Maladies NeurodegenerativesUMR 529333000 BordeauxFrance

The P2X4 receptor(P2X4)is an ATP-gated cation channel that is highly permeable to Ca2+and widely expressed in neuronal and glial cell types throughout the central nervous system(CNS).A growing body of evidence indicates that P2X4 plays key roles in numerous central disorders.P2X4 trafficking is highly regulated and consequently in normal situations,P2X4 is present on the plasma membrane at low density and found mostly within intracellular endosomal/lysosomal compartments.An increase in the de novo expression and/or surface density of P2X4 has been observed in microglia and/or neurons during pathological states.This review aims to summarize knowledge on P2X4 functions in CNS disorders and provide some insights into the relative contributions of neuronal and glial P2X4 in pathological contexts.However,determination of the cell-specific functions of P2X4 along with its intracellular and cell surface roles remain to be elucidated before its potential as a therapeutic target in multiple disorders can be defined.

关键词： purinergic signaling P2X ATP Ligandgated ion channels Chronic pain Brain trauma Ischemia Neurodegenerative diseases Alcohol Neuropsychiatric disorders

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The roles of microglia in viral encephalitis:from sensome to therapeutic targeting

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Cellular & Molecular Immunology 2021年第2期18卷 250-258页

作者： Chintan Chhatbar Marco Prinz Institute of Neuropathology Medical FacultyUniversity of FreiburgFreiburgGermany Center for Basics in NeuroModulation(NeuroModulBasics) Faculty of MedicineUniversity of FreiburgFreiburgGermany Signalling Research Centres BIOSS and CIBSS University of FreiburgFreiburgGermany

Viral encephalitis is a devastating disease with high mortality,and survivors often suffer from severe neurological complications.Microglia are innate immune cells of the central nervous system(CNS)parenchyma whose turnover is reliant on local proliferation.Microglia express a diverse range of proteins,which allows them to continuously sense the environment and quickly react to changes.Under inflammatory conditions such as CNS viral infection,microglia promote innate and adaptive immune responses to protect the host.However,during viral infection,a dysregulated microglia-T-cell interplay may result in altered phagocytosis of neuronal synapses by microglia that causes neurocognitive impairment.In this review,we summarize the current knowledge on the role of microglia in viral encephalitis,propose questions to be answered in the future and suggest possible therapeutic targets.

关键词： microglial activation viral encephalitis neurocognitive issues purinergic signaling PRR signaling

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Characterization of the Expression of the ATP-Gated P2X7 Receptor Following Status Epilepticus and during Epilepsy Using a P2X7-EGFP Reporter Mouse

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Neuroscience Bulletin 2020年第11期36卷 1242-1258页

作者： James Morgan Mariana Alves Giorgia Conte Aida Menendez-Mendez Laura de Diego-Garcia Gioacchino de Leo Edward Beamer Jonathon Smith Annette Nicke Tobias Engel Department of Physiology and Medical Physics Royal College of Surgeons in IrelandDublin D02 YN77Ireland FutureNeuro Science Foundation Ireland Research Centre for Chronic and Rare Neurological DiseasesRoyal College of Surgeons in IrelandDublin D02 YN77Ireland Walther Straub Institute of Pharmacology and Toxicology Faculty of MedicineLudwig-Maximilians-Universitat Miinchen80336 MunichGermany

Mounting evidence suggests that the ATP-gated P2X7 receptor contributes to increased hyperexcitability in the brain.While increased expression of P2X7 in the hippocampus and cortex following status epilepticus and during epilepsy has been repeatedly demonstrated,the cell type-specific expression of P2X7 and its expression in extra-hippocampal brain structures remains incompletely explored.In this study,P2X7 expression was visualized by using a transgenic mouse model overexpressing P2X7 fused to the fluorescent protein EGFP.The results showed increased P2X7-EGFP expression after status epilepticus induced by intra-amygdala kainic acid and during epilepsy in different brain regions including the hippocampus,cortex,striatum,thalamus and cerebellum,and this was most evident in microglia and oligodendrocytes.Colocalization of P2X7-EGFP with cell type-specific markers was not detected in neurons or astrocytes.These data suggest that P2X7 activation is a common pathological hallmark across different brain structures,possibly contributing to brain inflammation and neurodegeneration following acute seizures and during epilepsy.

关键词： purinergic signaling P2X7 Green fluorescence protein Status epilepticus Epilepsy Cell typespecific expression

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Enteric nervous system and inflammatory bowel diseases:Correlated impacts and therapeutic approaches through the P2X7 receptor

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World Journal of Gastroenterology 2021年第46期27卷 7909-7924页

作者： Henrique Inhauser Riceti Magalhães Patricia Castelucci Department of Surgery School of Veterinary Medicine and Animal SciencesUniversity of São PauloSão Paulo 08000-000Brazil Department of Anatomy Institute of Biomedical SciencesUniversity of São PauloSão Paulo 08000-000Brazil

The enteric nervous system(ENS)consists of thousands of small ganglia arranged in the submucosal and myenteric plexuses,which can be negatively affected by Crohn’s disease and ulcerative colitis-inflammatory bowel diseases(IBDs).IBDs are complex and multifactorial disorders characterized by chronic and recurrent inflammation of the intestine,and the symptoms of IBDs may include abdominal pain,diarrhea,rectal bleeding,and weight loss.The P2X7 receptor has become a promising therapeutic target for IBDs,especially owing to its wide expression and,in the case of other purinergic receptors,in both human and model animal enteric cells.However,little is known about the actual involvement between the activation of the P2X7 receptor and the cascade of subsequent events and how all these activities associated with chemical signals interfere with the functionality of the affected or treated intestine.In this review,an integrated view is provided,correlating the structural organization of the ENS and the effects of IBDs,focusing on cellular constituents and how therapeutic approaches through the P2X7 receptor can assist in both protection from damage and tissue preservation.

关键词： Chemical coding Enteric nervous system Gastroenterology Inflammatory bowel diseases P2X7 receptor purinergic signaling

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purinergic Modulation of Activity in the Developing Auditory Pathway

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Neuroscience Bulletin 2020年第11期36卷 1285-1298页

作者： Sasa Jovanovic Ivan Milenkovic School of Medicine and Health Sciences Carl von Ossietzky University Oldenburg26129 OldenburgGermany

purinergic P2 receptors,activated by endogenous ATP,are prominently expressed on neuronal and nonneuronal cells during development of the auditory periphery and central auditory neurons.In the mature cochlea,extracellular ATP contributes to ion homeostasis,and has a protective function against noise exposure.Here,we focus on the modulation of activity by extracellular ATP during early postnatal development of the lower auditory pathway.In mammals,spontaneous patterned activity is conveyed along afferent auditory pathways before the onset of acoustically evoked signal processing.During this critical developmental period,inner hair cells fire bursts of action potentials that are believed to provide a developmental code for synaptic maturation and refinement of auditory circuits,thereby establishing a precise tonotopic organization.Endogenous ATP-release triggers such patterned activity by raising the extracellular K+concentration and contributes to firing by increasing the excitability of auditory nerve fibers,spiral ganglion neurons,and specific neuron types within the auditory brainstem,through the activation of diverse P2 receptors.We review recent studies that provide new models on the contribution of purinergic signaling to early development of the afferent auditory pathway.Further,we discuss potential future directions of purinergic research in the auditory system.

关键词： purinergic signaling Auditory system Development Cochlea Spiral ganglion Auditory brainstem

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