LPS and TNF alpha modulate AMPA/NMDA receptor subunit expression and induce PGE2 and glutamate release in preterm fetal ovine mixed glial cultures

Journal of Neuroinflammation

Mhoyra Fraser¹  Laura Bennet¹  Murray D Mitchell²  Alistair J Gunn¹  Luke Weaver-Mikaere¹ 

[1] Department of Physiology, The University of Auckland, Auckland, New Zealand;University of Queensland Centre for Clinical Research, University of Queensland, Herston, QLD, Australia

关键词: in vitro;    COX-2;    MK801;    NBQX;    NMDA;    AMPA;    Pre-oligodendrocyte;    Inflammation;    Fetal Sheep;   

Others  :  834557
DOI  :  10.1186/1742-2094-10-153

 received in 2013-08-09, accepted in 2013-12-02,  发布年份 2013

【 摘 要 】

Background

White matter injury (WMI) is the major antecedent of cerebral palsy in premature infants, and is often associated with maternal infection and the fetal inflammatory response. The current study explores the therapeutic potential of glutamate receptor blockade or cyclooxygenase-2 (COX-2) inhibition for inflammatory WMI.

Methods

Using fetal ovine derived mixed glia cultures exposed to tumour necrosis factor-α (TNF-α) or lipopolysaccharide (LPS), the expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) and N-methyl D-aspartate (NMDA) glutamate receptors and their contribution to inflammation mediated pre-oligodendrocyte (OL) death was evaluated. The functional significance of TNF-α and COX-2 signalling in glutamate release in association with TNF-α and LPS exposure was also assessed.

Results

AMPA and NMDA receptors were expressed in primary mixed glial cultures on developing OLs, the main cell-type present in fetal white matter at a period of high risk for WMI. We show that glutamate receptor expression and configuration are regulated by TNF-α and LPS exposure, but AMPA and NMDA blockade, either alone or in combination, did not reduce pre-OL death. Furthermore, we demonstrate that glutamate and prostaglandin E2 (PGE2) release following TNF-α or LPS are mediated by a TNF-α-COX-2 dependent mechanism.

Conclusions

Overall, these findings suggest that glial-localised glutamate receptors likely play a limited role in OL demise associated with chronic inflammation, but supports the COX-2 pathway as a potential therapeutic target for infection/inflammatory-mediated WMI.

【 授权许可】

   
2013 Weaver-Mikaere et al.; licensee BioMed Central Ltd.

【 图 表 】

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