<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(1)</volume><submitter>Winerdal M</submitter><pubmed_abstract>Neonatal brain hypoxic ischemia (HI) often results in long-term motor and cognitive impairments. Post-ischemic inflammation greatly effects outcome and adenosine receptor signaling modulates both HI and immune cell function. Here, we investigated the influence of adenosine A1 receptor deficiency (A1R(-/-)) on key immune cell populations in a neonatal brain HI model. Ten-day-old mice were subjected to HI. Functional outcome was assessed by open locomotion and beam walking test and infarction size evaluated. Flow cytometry was performed on brain-infiltrating cells, and semi-automated analysis of flow cytometric data was applied. A1R(-/-) mice displayed larger infarctions (+33%, p &lt; 0.05) and performed worse in beam walking tests (44% more mistakes, p &lt; 0.05) than wild-type (WT) mice. Myeloid</pubmed_abstract><journal>Purinergic signalling</journal><pagination>89-101</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4749537</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Adenosine A1 receptors contribute to immune regulation after neonatal hypoxic ischemic brain injury.</pubmed_title><pmcid>PMC4749537</pmcid><pubmed_authors>Wang YQ</pubmed_authors><pubmed_authors>Fredholm BB</pubmed_authors><pubmed_authors>Winerdal M</pubmed_authors><pubmed_authors>Winerdal ME</pubmed_authors><pubmed_authors>Winqvist O</pubmed_authors><pubmed_authors>Aden U</pubmed_authors></additional><is_claimable>false</is_claimable><name>Adenosine A1 receptors contribute to immune regulation after neonatal hypoxic ischemic brain injury.</name><description>Neonatal brain hypoxic ischemia (HI) often results in long-term motor and cognitive impairments. Post-ischemic inflammation greatly effects outcome and adenosine receptor signaling modulates both HI and immune cell function. Here, we investigated the influence of adenosine A1 receptor deficiency (A1R(-/-)) on key immune cell populations in a neonatal brain HI model. Ten-day-old mice were subjected to HI. Functional outcome was assessed by open locomotion and beam walking test and infarction size evaluated. Flow cytometry was performed on brain-infiltrating cells, and semi-automated analysis of flow cytometric data was applied. A1R(-/-) mice displayed larger infarctions (+33%, p &lt; 0.05) and performed worse in beam walking tests (44% more mistakes, p &lt; 0.05) than wild-type (WT) mice. Myeloid</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Mar</publication><modification>2026-05-05T08:33:40.866Z</modification><creation>2019-03-27T02:08:56Z</creation></dates><accession>S-EPMC4749537</accession><cross_references><pubmed>26608888</pubmed><doi>10.1007/s11302-015-9482-3</doi></cross_references></HashMap>