Expression and localization of annexin A7 in the rat lithium-pilocarpine model of acquired epilepsy.
- Author:
Sheng-nian ZHOU
1
;
Cheng-shan LI
;
Li-qing LIU
;
Lan SHEN
;
Yan LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Annexin A7; analysis; physiology; Calcium; metabolism; Cerebral Cortex; chemistry; Disease Models, Animal; Fluorescent Antibody Technique; Hippocampus; chemistry; Immunohistochemistry; Lithium Chloride; Male; Pilocarpine; Rats; Rats, Wistar; Status Epilepticus; chemically induced; metabolism
- From: Chinese Medical Journal 2010;123(17):2410-2415
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDAnnexin A7 (synexin, ANXA7) is a member of annexins, which plays an essential role in the regulation of calcium homeostasis. Considerable evidence shows that the pathogenetic mechanism of acquired epilepsy (AE) has been related to the imbalance of calcium homeostasis. The aim of this study was to investigate ANXA7 expression and cellular localization in the cortex and hippocampus in the rat lithium-pilocarpine model of AE.
METHODSTotally 81 adult healthy male Wistar rats were randomly divided into control group (n = 9) and experimental group (n = 72), the experimental group contained eight subgroups according to sacrifice time (n = 9) (6-hour, 24-hour, 48-hour, 72-hour, 7-day, 15-day, 1-month, and 2-month). In the experimental group, rats were intraperitoneally injected by lithium-pilocarpine to induce AE model. We examined the expression and localization of ANXA7 via immunohistochemistry, double-label immunofluorescence with the use of neuron specific enolase (NSE) antibody, glial fibrillary acidic protein (GFAP) antibody and propidium iodide (PI), respectively. The data of optical density value were analyzed by analysis of variance.
RESULTSANXA7 expression increased significantly in the experimental groups especially in the acute period (6 hours, 24 hours, and 48 hours after the onset of seizure) using immunohistochemistry. Double-label immunofluorescence and confocal microscopy disclosed that ANXA7 localized in the neurons but not in astrocytes and did not localize in the nucleus, which were performed with anti-NSE, anti-GFAP and PI respectively.
CONCLUSIONANXA7 may play a potential role in the pathogenetic mechanisms of the rat lithium-pilocarpine model of AE.