Effect of synchronous perfusion of NaN3 in changes in content of cholinergic neurotransmitter in medial prefrontal cortex and hippocampal extra-cellular fluid.
- Author:
Mei-Yu ZHANG
;
Dan-Dan SUN
;
Yang LIU
;
Yue CUI
;
Xiao-Liang ZHAO
;
Ying ZHANG
;
Zhi-Guo WANG
;
Dan-Qiao WANG
- Publication Type:Journal Article
- MeSH: Acetylcholine; metabolism; Animals; Choline; metabolism; Extracellular Fluid; drug effects; metabolism; Hippocampus; cytology; Male; Neurotransmitter Agents; metabolism; Perfusion; Prefrontal Cortex; cytology; Rats; Rats, Sprague-Dawley; Sodium Azide; administration & dosage; pharmacology; Time Factors
- From: China Journal of Chinese Materia Medica 2014;39(3):488-492
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of synchronous perfusion of specific respiratory chain complex IV inhibitor sodium azide (NaN3) in brain on rat ventromedial prefrontal cortex (mPFC) and acetylcholine (ACh) and choline (Ch) contents in hippocampal extra-cellular fluid, and establish the AD rat model induced by mitochondrial acute injury.
METHODThe synchronous dual-probe dual-channel brain microdialysis sampling technology was applied to synchronously perfuse modified Ringer's solution containing NaN3 (50 micro mol L-1) and neostigmine (2 micro mol L-1) into mPFC and hippocampus of conscious, freely moving normal rats, and continuously collect dialysates from different encephalic areas. Dynamic contents of ACh and Ch were determined by high performance liquid chromatography-post-column immobilized enzyme reactor-electrochemical process.
RESULTACh and Ch contents in mPFC extracellular fluid of normal rats were higher than that in hippocampus. During the process of perfusion, NaN3 could significantly reduce ACh in mPFC/hippocampal extra-cellular fluid, but remarkably increase Ch, and constantly inhibit the recovery of ACh and Ch contents in mPFC/hippocampus.
CONCLUSIONThe synchronous perfusion of NaN3in rat mPFC and hippocampus can injure functions of the cholinergic nerve projection area, and cause the acute AD model with ACh and Ch metabolic disorders. This model can be used in pathogenetic and pharmacological studies.