{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T09:49:39Z","timestamp":1790675379799,"version":"4.1.0"},"reference-count":69,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T00:00:00Z","timestamp":1334620800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Purpose:\u2002<\/jats:bold>The endocannabinoid system is known to modulate seizure activity in several in vivo and in vitro models, and CB<jats:sub>1<\/jats:sub>\u2010receptor activation is anticonvulsant in the rat pilocarpine model of acquired epilepsy (AE). In these epileptic rats, a unique redistribution of the CB<jats:sub>1<\/jats:sub>receptor occurs within the hippocampus; however, an anatomically inclusive analysis of the effect of status epilepticus (SE)\u2013induced AE on CB<jats:sub>1<\/jats:sub>receptors has not been thoroughly evaluated. Therefore, statistical parametric mapping (SPM), a whole\u2010brain unbiased approach, was used to study the long\u2010term effect of pilocarpine\u2010induced SE on CB<jats:sub>1<\/jats:sub>\u2010receptor binding and G\u2010protein activation in rats with AE.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold>Serial coronal sections from control and epileptic rats were cut at equal intervals throughout the neuraxis and processed for [<jats:sup>3<\/jats:sup>H]WIN55,212\u20102 (WIN) autoradiography, WIN\u2010stimulated [<jats:sup>35<\/jats:sup>S]GTP\u03b3S autoradiography, and CB<jats:sub>1<\/jats:sub>\u2010receptor immunohistochemistry (IHC). The autoradiographic techniques were evaluated with both region of interest (ROI) and SPM analyses.<\/jats:p><jats:p><jats:bold>Key Findings:\u2002<\/jats:bold>In rats with AE, regionally specific increases in CB<jats:sub>1<\/jats:sub>\u2010receptor binding and activity were detected in cortex, discrete thalamic nuclei, and other regions including caudate\u2010putamen and septum, and confirmed by IHC. However, CB<jats:sub>1<\/jats:sub>receptors were unaltered in several brain regions, including substantia nigra and cerebellum, and did not exhibit regional decreases in rats with AE.<\/jats:p><jats:p><jats:bold>Significance:\u2002<\/jats:bold>This study provides the first comprehensive evaluation of the regional distribution of changes in CB<jats:sub>1<\/jats:sub>\u2010receptor expression, binding, and G\u2010protein activation in the rat pilocarpine model of AE. These regions may ultimately serve as targets for cannabinomimetic compounds or manipulation of the endocannabinoid system in epileptic brain.<\/jats:p>","DOI":"10.1111\/j.1528-1167.2012.03460.x","type":"journal-article","created":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T15:09:21Z","timestamp":1334675361000},"page":"897-907","source":"Crossref","is-referenced-by-count":9,"title":["Statistical parametric mapping reveals regional alterations in cannabinoid CB<sub>1<\/sub>receptor distribution and G\u2010protein activation in the 3D reconstructed epileptic rat brain"],"prefix":"10.1111","volume":"53","author":[{"given":"Katherine W.","family":"Sayers","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter T.","family":"Nguyen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert 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