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Mouse α 1B ‐adrenergic receptor is expressed in neurons and NG2 oligodendrocytes
Author(s) -
Papay Robert,
Gaivin Robert,
McCune Dan F.,
Rorabaugh Boyd R.,
Macklin Wendy B.,
McGrath John C.,
Perez Dianne M.
Publication year - 2004
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20215
Subject(s) - biology , neuroscience , receptor , adrenergic receptor , genetics
α 1 ‐Adrenergic receptors (ARs) are well‐known mediators of the sympathetic nervous system, are highly abundant in the brain, but are the least understood in the central nervous system. The particular cell types in the brain that contain these receptors or their functions are not known because of the lack of high avidity antibodies and selective ligands. We developed transgenic mice that endogenously overexpress the α 1B ‐AR subtype fused with the enhanced green fluorescent protein (EGFP). Endogenous expression was obtained by using a 3.4 kb fragment of the mouse α 1B ‐AR promoter. Using this model, we determined cellular localization of the α 1B ‐AR throughout the brain. The α 1B ‐AR‐EGFP fusion protein is expressed in neurons throughout the brain and in the Purkinje cells of the cerebellum. The α 1B ‐AR is also expressed in NG2 oligodendrocyte precursor cells in both neonatal cell cultures and in the adult cerebral cortex, but is weakly expressed in mature oligodendrocytes. The α 1B ‐AR was not observed in astrocytes or in cerebral vascular smooth muscle, cell types previously suggested to contain α 1 ‐ARs. We conclude that the α 1B ‐AR is highly abundant throughout the brain, predominately in neurons, and may be involved in the development of the oligodendrocyte. In adult NG2 cells, implicated in stem cell‐like functions, the α 1B ‐AR may also play a role. This is the first report of a transgenic tagged‐GPCR approach to determine in vivo localization of a receptor. J. Comp. Neurol. 478:1–10, 2004. © 2004 Wiley‐Liss, Inc.

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