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Adenosine A2A Receptors in Bone Marrow-Derived Cells But Not in Forebrain Neurons Are Important Contributors to 3-Nitropropionic Acid-Induced Striatal Damage as Revealed by Cell-Type-Selective Inactivation.
- Source :
- Journal of Neuroscience; 11/1/2006, Vol. 26 Issue 44, p7-7, 1p
- Publication Year :
- 2006
-
Abstract
- Endogenous adenosine acting at the adenosine A<subscript>2A</subscript> receptor (A<subscript>2A</subscript>R) can modify brain injury in a variety of neurological disorder models. However, both A<subscript>2A</subscript>R activation and inactivation have been shown to be neuroprotective in different situations, raising the intriguing possibility that A<subscript>2A</subscript>Rs in distinct cellular elements may have different and even opposing effects. In this study, we developed three novel transgenic models to dissect out cell-type-specific actions of A<subscript>2A</subscript>Rs on striatal damage by the mitochondrial toxin 3-nitropropionic acid (3-NP). Whereas global inactivation of A<subscript>2A</subscript>Rs exacerbated 3-NP-induced neurological deficit behaviors and striatal damage, selective inactivation of A<subscript>2A</subscript>Rs in forebrain neurons (using the Cre/loxP strategy) did not affect neurological deficit or striatal damage after the acute systemic treatment of 3-NP and intrastriatal injection of malonate. However, selective inactivation of A<subscript>2A</subscript>Rs in bone marrow-derived cells (BMDCs) by transplanting bone marrow cells from global A<subscript>2A</subscript>R knock-out (KO) mice into wild-type C57BL/6 mice produced a similar phenotype of global A<subscript>2A</subscript>R KO mice, i.e., exacerbation of 3-NP-induced striatal damage. Thus, cell-type-selective inactivation of A<subscript>2A</subscript>Rs reveals that A<subscript>2A</subscript>Rs in BMDCs but not in forebrain neurons are an important contributor to striatal damage induced by mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]
- Subjects :
- ADENOSINES
PROPIONIC acid
NEURONS
BONE marrow
CELLS
Subjects
Details
- Language :
- English
- ISSN :
- 02706474
- Volume :
- 26
- Issue :
- 44
- Database :
- Complementary Index
- Journal :
- Journal of Neuroscience
- Publication Type :
- Academic Journal
- Accession number :
- 23193382