{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T17:56:42Z","timestamp":1787162202056,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2011,2,2]],"date-time":"2011-02-02T00:00:00Z","timestamp":1296604800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Changes in the regional distribution of the metabotropic GABA type B receptors (GABA\n                    <jats:sub>B<\/jats:sub>\n                    ) were investigated in a rat model of Huntignton's disease. Animals received a unilateral intrastriatal injection of quinolinic acid (QA), and GABA\n                    <jats:sub>B<\/jats:sub>\n                    immunoreactivity was monitored 3, 11, and 21 days postinjection in the striatum and substantia nigra (SN). Two antibodies, recognizing either the GABA\n                    <jats:sub>B1<\/jats:sub>\n                    or the GABA\n                    <jats:sub>B2<\/jats:sub>\n                    receptor subtypes, were used. QA injection rapidly induced a protracted increase in GABA\n                    <jats:sub>B1<\/jats:sub>\n                    or GABA\n                    <jats:sub>B2<\/jats:sub>\n                    immunoreactivity in the lesioned striatum, despite the neuronal loss. In the SN, a continuous increase in GABA\n                    <jats:sub>B1<\/jats:sub>\n                    and GABA\n                    <jats:sub>B2<\/jats:sub>\n                    immunoreactivity was observed at all time points in the ipsilateral pars reticulata (SNr), whereas the pars compacta (SNc) was unaffected by this phenomenon. This increase was supported by a densitometric analysis. At day 21 postlesion induction, intensely labeled stellate cells and processes were found in the ipsilateral SNr, in addition to immunoreactive neurons. Double labeling of GABA\n                    <jats:sub>B1<\/jats:sub>\n                    and glial fibrillary acidic protein (GFAP) showed that the stellate cells were reactive astrocytes. Hence, part of the sustained increase in GABA\n                    <jats:sub>B<\/jats:sub>\n                    immunoreactivity that takes place in the SNr and possibly the striatum may be ascribed to reactive astrocytes. It is suggested that GABA\n                    <jats:sub>B<\/jats:sub>\n                    receptors are up\u2010regulated in these reactive astrocytes and that agonists might influence the extent of this astroglial reaction. \u00a9 2011 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jnr.22574","type":"journal-article","created":{"date-parts":[[2011,2,2]],"date-time":"2011-02-02T13:47:45Z","timestamp":1296654465000},"page":"524-535","source":"Crossref","is-referenced-by-count":10,"title":["\u03b3\u2010Aminobutyric acid type B receptor changes in the rat striatum and substantia nigra following intrastriatal quinolinic acid 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