{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T20:34:52Z","timestamp":1786739692452,"version":"build-2736575974"},"reference-count":33,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    During brain ischemia, excitotoxicity and peri-infarct depolarization injuries occur and cause cerebral tissue damage. Indeed, anoxic depolarization, consisting of massive neuronal depolarization due to the loss of membrane ion gradients, occurs\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    or\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    during an energy failure. The neuromodulator adenosine is released in huge amounts during cerebral ischemia and exerts its effects by activating specific metabotropic receptors, namely: A\n                    <jats:sub>1<\/jats:sub>\n                    , A\n                    <jats:sub>2A<\/jats:sub>\n                    , A\n                    <jats:sub>2B<\/jats:sub>\n                    , and A\n                    <jats:sub>3<\/jats:sub>\n                    . The A\n                    <jats:sub>2A<\/jats:sub>\n                    receptor subtype is highly expressed in striatal medium spiny neurons, which are particularly susceptible to ischemic damage. Evidence indicates that the A\n                    <jats:sub>2A<\/jats:sub>\n                    receptors 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 hours. We recently added new knowledge to the mechanisms by which the adenosine A\n                    <jats:sub>2A<\/jats:sub>\n                    receptor 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 deprivation. We demonstrated that the selective block of A\n                    <jats:sub>2A<\/jats:sub>\n                    receptors 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\n                    <jats:sup>+<\/jats:sup>\n                    channel modulation and a presynaptic inhibition of glutamate release by the A\n                    <jats:sub>2A<\/jats:sub>\n                    receptor antagonist. The present review summarizes the latest findings in the literature about the possibility of developing selective ligands of A\n                    <jats:sub>2A<\/jats:sub>\n                    receptors as advantageous therapeutic tools that may contribute to counteracting neurodegeneration after brain ischemia.\n                  <\/jats:p>","DOI":"10.4103\/1673-5374.375309","type":"journal-article","created":{"date-parts":[[2023,5,25]],"date-time":"2023-05-25T08:10:01Z","timestamp":1685002201000},"page":"255-257","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":10,"title":["Adenosine A2A receptor blockade attenuates excitotoxicity in rat striatal medium spiny neurons during an ischemic-like insult"],"prefix":"10.4103","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4434-5919","authenticated-orcid":false,"given":"Elisabetta","family":"Coppi","sequence":"first","affiliation":[{"name":"Department of 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