γ-Aminobutyric acid type B receptor changes in the rat striatum and substantia nigra following intrastriatal quinolinic acid lesions

Changes in the regional distribution of the metabotropic GABA type B receptors (GABAB) were investigated in a rat model of Huntignton's disease. Animals received a unilateral intrastriatal injection of quinolinic acid (QA), and GABAB immunoreactivity was monitored 3, 11, and 21 days postinjection in the striatum and substantia nigra (SN). Two antibodies, recognizing either the GABAB1 or the GABAB2 receptor subtypes, were used. QA injection rapidly induced a protracted increase in GABAB1 or GABAB2 immunoreactivity in the lesioned striatum, despite the neuronal loss. In the SN, a continuous increase in GABAB1 and GABAB2 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 GABAB1 and glial fibrillary acidic protein (GFAP) showed that the stellate cells were reactive astrocytes. Hence, part of the sustained increase in GABAB immunoreactivity that takes place in the SNr and possibly the striatum may be ascribed to reactive astrocytes. It is suggested that GABAB receptors are up‐regulated in these reactive astrocytes and that agonists might influence the extent of this astroglial reaction. © 2011 Wiley‐Liss, Inc.