Roles of glutamate receptor 2 and cellular free calcium in the pathogenesis of periventricular leukomalacia.
- Author:
Jing SHI
1
;
Yu-Jia YAO
;
Jin-Hui LI
;
De-Yuan LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Calcium; physiology; Humans; Infant, Newborn; Leukomalacia, Periventricular; etiology; Oligodendroglia; pathology; RNA, Messenger; analysis; Rats; Rats, Sprague-Dawley; Receptors, AMPA; genetics; physiology; Reverse Transcriptase Polymerase Chain Reaction
- From: Chinese Journal of Contemporary Pediatrics 2007;9(4):313-316
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the expression of the AMPA receptor subunit glutamate receptor 2 (GluR2) and the cellular free calcium concentration in the white matter of neonatal rats with periventricular leukomalacia (PVL) and their roles in the pathogenesis of PVL.
METHODSA PVL model was prepared by unilateral carotid artery ligation (UCL) followed by exposure to 6% oxygen for 4 hrs in 2-day-old rats. The neonatal rats performed a sham operation, without hypoxia-ischemia (HI), were used as the control group. At 12, 24, 48 and 72 hrs of HI, the expressions of GluR2 mRNA and protein in the white matter were detected using real time quantitative PCR and Western blot respectively. Spectrophotofluorimetry and Fura 2/AM were used to detect the cellular free calcium concentration.
RESULTSThe expressions of GluR2 mRNA and protein in the white matter were significantly reduced in the PVL group at 24 hrs of HI, and remained at lower expressions until 72 hrs of HI compared with the control group (P < 0.05). The cellular free calcium concentrations increased significantly in the PVL group at 12 hrs of HI, and remained at higher levels until 72 hrs of HI compared with the control group (P < 0.05).
CONCLUSIONSThe expressions of GluR2 mRNA and protein in the white matter decreased whereas the cellular free calcium concentration increased in neonatal rats with PVL. The decreased expression of GluR2 might lead to the overloading of cellular calcium in the white matter, which may cause neuronal damage and death.