Cellular localization of the full-length isoform of the type 2 corticotropin releasing factor receptor in the postnatal mouse cerebellar cortex

✍ Scribed by Kyung-Hoon Lee; Georgia A. Bishop; Jin Bin Tian; Yoon-Jin Jang; Bao Chi Bui; Truong Le Xuan Nguyen; Jee-Yin Ahn; James S. King

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 660 KB
• Volume: 85
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.21333

✦ Synopsis

Abstract

Corticotropin releasing factor (CRF) and its cognate receptors, defined as Type 1 and Type 2 have been localized within the cerebellum. The Type 2 CRF receptor (CRF‐R2) is known to have both a full length (CRF‐R2α) and a truncated (CRF‐R2α‐tr) isoform. A recent study documented CRF‐R2α primarily in Bergann glia and astrocytes, as well as in populations of Purkinje cells in the adult cerebellum. The goal of the present study is to determine if CRF‐R2α is present in the postnatal cerebellum, and if so to describe its cellular distribution. RT‐PCR data showed that CRF‐R2α is expressed in the mouse cerebellum from birth through postnatal day 21. Between birth and P14, CRF‐R2α‐immunoreactivity was localized within the somata of Purkinje cells, and migrating GABAergic interneurons. GFAP‐immunoreactive astrocytes, including Bergmann glia, also expressed CRF‐R2α‐immunoreactivity from P3‐P14. There is a change, however, in CRF‐R2α immunolabeling within neurons as the cerebellum matures. Compared to its expression in the adult cerebellum, Purkinje cells, and GABAergic interneurons showed more extensive CRF‐R2α immunolabeling during early postnatal development. We postulate that CRF‐R2α could be involved in developmental events related to the survival and differentiation of Purkinje cells and GABAergic neurons, whereas in the adult, this isoform of the CRF receptor family is likely involved in modulating Bergmann glia that have been shown to play a role in regulating the synaptic environment around Purkinje neurons. © 2007 Wiley‐Liss, Inc.