Penehyclidine hydrochloride inhibits glutamate release and related research in global brain ischemia/reperfusion rats.
- Author:
You SHANG
1
;
Pei-fei GU
;
Yu SHANG
;
Yue LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; metabolism; physiopathology; CA1 Region, Hippocampal; metabolism; Cholinergic Antagonists; pharmacology; Glutamic Acid; metabolism; Male; Quinuclidines; pharmacology; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; metabolism; Reperfusion Injury; metabolism; prevention & control
- From: Chinese Journal of Applied Physiology 2011;27(3):353-356
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of penehyclidine hydrochloride on glutamate (Glu)release and N-methyl-D-aspartate receptor (NMDAR)1 expression in hippocampus CA1 with global cerebral ischemia/reperfusion rats.
METHODSSixty male Wistar rats were randomly allocated into three groups; group A received sham operation; group B received ischemia/reperfusion; group C received penehyclidine hydrochloride treatment (2 mg/kg) before ischemia/reperfusion (n=20). Global cerebral ischemia was induced according to Pulsinelli-Brierley method. All animals were divided into two experiments: (I) Microdialysis plus HPLC/FD were used to detect Glu level after reperfusion 1 h, 3 h, 6 h. (II) After reperfusion 3 h, the animals were decapitated on ice and the brains were immediately removed to detect NMDAR1 expression in CA1 area by immunohistochemistry.
RESULTSAfter penehyclidine hydrochloride treatment, extracellular Glu level in CA1 were significantly decreased compared with those of control group (P < 0.05 or 0.01); Total integrated OD, average gray value and positive-cell area of NMDAR1 in CA1 were also significantly decreased compared with those of control group (P < 0.05 or 0.01).
CONCLUSIONPenehyclidine hydrochloride might has protective effect in hippocampus CA1 on global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting Glu release and NMDAR1 expression.