<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nesbitt KM</submitter><funding>NIMH NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>8173-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3799822</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>85(17)</volume><pubmed_abstract>Microdialysis sampling in the brain is employed frequently in the chemical analysis of neurological function and disease, but implanting the probes, which are substantially larger than the size and spacing of brain cells and blood vessels, is injurious and triggers ischemia, gliosis, and cell death at the sampling site. The nature of the interface between the brain and the microdialysis probe is critical to the use of microdialysis as a neurochemical analysis technique. The objective of the work reported here was to investigate the potential of two compounds, dexamethasone, a glucocorticoid anti-inflammatory agent, and XJB-5-131, a mitochondrially targeted reactive oxygen species scavenger, to mitigate the penetration injury. Measurements were performed in the rat brain striatum, which is </pubmed_abstract><journal>Analytical chemistry</journal><pubmed_title>Pharmacological mitigation of tissue damage during brain microdialysis.</pubmed_title><pmcid>PMC3799822</pmcid><funding_grant_id>R21 NS081744</funding_grant_id><funding_grant_id>P50 GM067082</funding_grant_id><funding_grant_id>MH 075989</funding_grant_id><funding_grant_id>R01 MH075989</funding_grant_id><funding_grant_id>NS 081744</funding_grant_id><pubmed_authors>Skoda EM</pubmed_authors><pubmed_authors>Michael AC</pubmed_authors><pubmed_authors>Nesbitt KM</pubmed_authors><pubmed_authors>Wipf P</pubmed_authors><pubmed_authors>Jaquins-Gerstl A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pharmacological mitigation of tissue damage during brain microdialysis.</name><description>Microdialysis sampling in the brain is employed frequently in the chemical analysis of neurological function and disease, but implanting the probes, which are substantially larger than the size and spacing of brain cells and blood vessels, is injurious and triggers ischemia, gliosis, and cell death at the sampling site. The nature of the interface between the brain and the microdialysis probe is critical to the use of microdialysis as a neurochemical analysis technique. The objective of the work reported here was to investigate the potential of two compounds, dexamethasone, a glucocorticoid anti-inflammatory agent, and XJB-5-131, a mitochondrially targeted reactive oxygen species scavenger, to mitigate the penetration injury. Measurements were performed in the rat brain striatum, which is </description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Sep</publication><modification>2025-04-04T19:30:10.576Z</modification><creation>2019-03-27T01:17:19Z</creation></dates><accession>S-EPMC3799822</accession><cross_references><pubmed>23927692</pubmed><doi>10.1021/ac401201x</doi></cross_references></HashMap>