The increased expression of metabotropic glutamate receptor 5 in subventricular zone neural progenitor cells and enhanced neurogenesis in a rat model of intracerebral hemorrhage.

The metabotropic glutamate receptor 5 (mGluR5) is closely relative to the proliferation, survival, and differentiation of neural progenitor cells (NPCs). This study primarily examined the mGluR5 expression of NPCs in subventricular zone (SVZ) and the effects of mGluR5 on neurogenesis to intracerebral hemorrhage (ICH) rat. The experiment was designated as the following: (1) The ICH model was established by collagenase infusion into the right striatum of the rats, and the brain tissue was collected to assess the expression of mGluR5 in SVZ NPCs. (2) The rat brains were sampled for immunostaining of doublecortin (DCX) and 5-bromo-2'-deoxyuridine (BrdU) to examine the effects of the (R,S)-2-chloro-5-hydroxyphenylglycine (CHPG) on neurogenesis. (3) Behavioral testing was carried out to evaluate the effects of CHPG on neurofunctional recovery. The results of Western blot analysis showed that mGluR5 levels in the ipsilateral SVZ increased as early as at 3 days after ICH, peaked at 14 days. The change of mGluR5 mRNA level in the ipsilateral SVZ was generally similar to the pattern of Western blot analysis. The immunostaining also demonstrated that some nestin-positive cells were co-expressed with mGluR5. The injection of CHPG into ipsilateral ventricle increased DCX levels both in the ipsilateral striatum (STR) and the peri-lesion area of the striatum (PLA). Meanwhile, a significant difference in behavioral score was presented at 28 days after ICH between the CHPG-treated rats and the vehicle-treated or the non-treated rats. Our results demonstrated for the first time that the increased expression of mGluR5 in SVZ NPCs occurred in ICH rat. The CHPG promoted the neurogenesis and improved neurofunctional symptom induced by ICH. These results suggested that the increased expression of mGluR5 on NPCs in SVZ may play an important role in neurogenesis in ICH rat.