http://www.nitrc.org/forum/forum.php?forum_id=7339 <table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="https://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&amp;cmd=Link&amp;LinkName=pubmed_pubmed&amp;from_uid=28382543">Related Articles</a></td></tr></table> <p><b>The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation.</b></p> <p>Psychopharmacology (Berl). 2017 Apr 05;:</p> <p>Authors: Sahlholm K, Ielacqua GD, Xu J, Jones LA, Schlegel F, Mach RH, Rudin M, Schroeter A</p> <p>Abstract<br/> RATIONALE: The dopamine D2 receptor (D2R) couples to inhibitory Gi/o proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied D2R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo.<br/> OBJECTIVES: The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies D2R-dependent responses.<br/> METHODS: fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the D2R antagonist, eticlopride.<br/> RESULTS: Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes.<br/> CONCLUSIONS: The prolonged striatal response decay rates in KO animals might reflect impaired D2R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of D2R.<br/> </p><p>PMID: 28382543 [PubMed - as supplied by publisher]</p> en-us Copyright 2000-2026 NITRC OSI Wed, 06 May 2026 15:45:31 GMT http://blogs.law.harvard.edu/tech/rss NITRC RSS generator