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Adenosine A_(2A)receptor blockade attenuates excitotoxicity in rat striatal medium spiny neurons during an ischemic-like insult

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Neural Regeneration Research 2024年第2期19卷 255-257页

作者： Elisabetta Coppi Federica Cherchi Alasdair J.Gibb Department of Neuroscience PsychologyDrug Research and Child HealthUniversity of FlorenceFlorenceItaly Department of Neuroscience Physiology and PharmacologyUniversity College LondonLondonUK

During brain ischemia,excitotoxicity and peri-infarct depolarization injuries occur and cause cerebral tissue ***,anoxic depolarization,consisting of massive neuronal depolarization due to the loss of membrane ion gradients,occurs in vivo or in vitro during an energy *** neuromodulator adenosine is released in huge amounts during cerebral ischemia and exerts its effects by activating specific metabotropic receptors,namely:A_(1),A_(2A),A_(2B),and A_(3).The A_(2A)receptor subtype is highly expressed in striatal medium spiny neurons,which are particularly susceptible to ischemic *** indicates that the A2Areceptors are upregulated in the rat striatum after stroke and the selective antagonist SCH58261 protects from exaggerated glutamate release within the first 4 hours from the insult and alleviates neurological impairment and histological injury in the following 24 *** recently added new knowledge to the mechanisms by which the adenosine A2Areceptor subtype participates in ischemia-induced neuronal death by performing patch-clamp recordings from medium spiny neurons in rat striatal brain slices exposed to oxygen and glucose *** demonstrated that the selective block of A2Areceptors by SCH58261 significantly reduced ionic imbalance and delayed the anoxic depolarization in medium spiny neurons during oxygen and glucose deprivation and that the mechanism involves voltage-gated K+channel modulation and a presynaptic inhibition of glutamate release by the A2Areceptor *** present review summarizes the latest findings in the literature about the possibility of developing selective ligands of A2Areceptors as advantageous therapeutic tools that may contribute to counteracting neurodegeneration after brain ischemia.

关键词： adenosine A_(2A)receptors anoxic depolarization brain ischemia glutamate excitotoxicity medium spiny neurons oxygen and glucose deprivation

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Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia-reperfusion injury

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Acta Pharmaceutica Sinica B 2020年第9期10卷 1634-1645,1802页

作者： Xiaoling Chen Jingliang Zhang Yan Song Pan Yang Yang Yang Zhuo Huang Kewei Wang Department of Molecular and Cellular Pharmacology State Key Laboratory of Natural and Biomimetic DrugsPeking University School of Pharmaceutical SciencesBeijing 100191China Department of Pharmacology Qingdao University School of PharmacyQingdao 266021China Department of Medicinal Chemistry and Molecular Pharmacology Purdue University College of PharmacyWest LafayetteIN 47907USA Institute of Innovative Drugs Qingdao University School of PharmacyQingdao 266021China

Systematic administration of anti-inflammatory cytokine interleukin 4(IL-4)has been shown to improve recovery after cerebral ischemic ***,whether IL-4 affects neuronal excitability and how IL-4 improves ischemic injury remain largely *** we report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia-repertusion(I/R)*** multi-electrode array(MEA)recordings,IL-4 reduces spontaneous firings and network activities of mouse primary cortical ***-4 mRNA and protein expressions are upregulated after I/R *** deletion of 11-4 gene aggravates I/R injury in vivo and exacerbates oxygen-glucose deprivation(OGD)injury in cortical ***,supplemental IL-4 protects 11-4-/-cortical neurons against OGD ***,cortical pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic hyperexcitability and enhanced excitatory synaptic transmissions in Il-4-/-***,upregulation of Nav1.1 channel,and downregulations of KCa3.1 channel and a6 subunit of GABAA receptors are detected in the cortical tissues and primary cortical neurons from Il-4-/-*** together,our findings demonstrate that IL-4 deficiency results in neural hyperexcitability and aggravates I/R injury,thus activation of IL-4 signaling may protect the brain against the development of permanent damage and help recover from ischemic injury after stroke.

关键词： anoxic depolarization IL-4 Ischemia-reperfusion injury Neuronal excitability Synaptic transmissions

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