<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Morgan J</submitter><funding>Research Foundation</funding><funding>MCIN/AEI/10.13039/501100011033</funding><funding>European Union</funding><funding>Horizon 2020 Framework Programme</funding><funding>Science Foundation Ireland</funding><funding>Irish Research Council for Science, Engineering and Technology</funding><funding>ASCRS Research Foundation</funding><funding>Horizon 2020</funding><funding>European Commission</funding><funding>H2020 Marie Skłodowska-Curie Actions</funding><funding>European Regional Development Fund</funding><pagination>511-523</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10108015</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>64(2)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>The P2X7 receptor (P2X7R) is an important contributor to neuroinflammation, responding to extracellularly released adenosine triphosphate. Expression of the P2X7R is increased in the brain in experimental and human epilepsy, and genetic or pharmacologic targeting of the receptor can reduce seizure frequency and severity in preclinical models. Experimentally induced seizures also increase levels of the P2X7R in blood. Here, we tested &lt;sup>18&lt;/sup> F-JNJ-64413739, a positron emission tomography (PET) P2X7R antagonist, as a potential noninvasive biomarker of seizure-damage and epileptogenesis.&lt;h4>Methods&lt;/h4>Status epilepticus was induced via an intra-amygdala microinjection of kainic acid. Static PET studies (30 min duration, initiated 30 min after tracer administration) we</pubmed_abstract><journal>Epilepsia</journal><pubmed_title>Increased uptake of the P2X7 receptor radiotracer &lt;sup>18&lt;/sup> F-JNJ-64413739 in the brain and peripheral organs according to the severity of status epilepticus in male mice.</pubmed_title><pmcid>PMC10108015</pmcid><funding_grant_id>766124</funding_grant_id><funding_grant_id>MDM-2017-0720</funding_grant_id><funding_grant_id>GOIPD/2020/865</funding_grant_id><funding_grant_id>16/RC/3948</funding_grant_id><funding_grant_id>884956</funding_grant_id><funding_grant_id>PID2020-117656RB-I00</funding_grant_id><funding_grant_id>17/CDA/4708</funding_grant_id><pubmed_authors>Morgan J</pubmed_authors><pubmed_authors>Leister H</pubmed_authors><pubmed_authors>Gomez-Vallejo V</pubmed_authors><pubmed_authors>Engel T</pubmed_authors><pubmed_authors>Alves M</pubmed_authors><pubmed_authors>Henshall DC</pubmed_authors><pubmed_authors>Smith J</pubmed_authors><pubmed_authors>Visekruna A</pubmed_authors><pubmed_authors>Melia C</pubmed_authors><pubmed_authors>Bhattacharya A</pubmed_authors><pubmed_authors>Menendez Mendez A</pubmed_authors><pubmed_authors>Baz Z</pubmed_authors><pubmed_authors>Ceusters M</pubmed_authors><pubmed_authors>Nicke A</pubmed_authors><pubmed_authors>Moreno O</pubmed_authors><pubmed_authors>Llop J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Increased uptake of the P2X7 receptor radiotracer &lt;sup>18&lt;/sup> F-JNJ-64413739 in the brain and peripheral organs according to the severity of status epilepticus in male mice.</name><description>&lt;h4>Objective&lt;/h4>The P2X7 receptor (P2X7R) is an important contributor to neuroinflammation, responding to extracellularly released adenosine triphosphate. Expression of the P2X7R is increased in the brain in experimental and human epilepsy, and genetic or pharmacologic targeting of the receptor can reduce seizure frequency and severity in preclinical models. Experimentally induced seizures also increase levels of the P2X7R in blood. Here, we tested &lt;sup>18&lt;/sup> F-JNJ-64413739, a positron emission tomography (PET) P2X7R antagonist, as a potential noninvasive biomarker of seizure-damage and epileptogenesis.&lt;h4>Methods&lt;/h4>Status epilepticus was induced via an intra-amygdala microinjection of kainic acid. Static PET studies (30 min duration, initiated 30 min after tracer administration) we</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2026-05-02T11:19:11.188Z</modification><creation>2024-11-06T21:28:13.4Z</creation></dates><accession>S-EPMC10108015</accession><cross_references><pubmed>36507708</pubmed><doi>10.1111/epi.17484</doi></cross_references></HashMap>