Involvement of the paraventricular nucleus in the occurrence of arrhythmias in middle cerebral artery occlusion rats.
BACKGROUND
Ischemic stroke complicating with arrhythmia is one of the main causes of sudden death. To investigate the association between ischemic stroke-induced arrhythmia and the activity of paraventricular nucleus (PVN), we used Fos protein as an objective indicator to illustrate the functional state of PVN neurons in middle cerebral artery occlusion (MCAO) rats, in single intracerebroventricular injection of l-glutamate rats and in application of MK-801 before l-glutamate injection and MCAO rats.


METHODS
The standard limb II electrocardiography was continuously recorded by a biological signal collecting and processing system. The experimental cerebral ischemic animal model was established by occluding the right middle cerebral artery. The Fos protein expression was detected by immunohistochemistry and Western blot.


RESULTS
The incidence of arrhythmia was significantly higher than that of controls (75.89% versus 0%), and Fos protein expression in the PVN also increased significantly in MCAO rats; both of them could be blocked by prior application of MK-801. Intracerebroventricular injection of l-glutamate induced changes in Fos protein expression and arrhythmia similar to that in the stroke, which could also be blocked by prior application of MK-801.


CONCLUSIONS
It was concluded that activation of the PVN in MCAO rats is likely mediated by glutamate via activation of N-methyl-D-aspartic acid (NMDA) receptors, which causes arrhythmias.
Department of Physiology, Harbin Medical University, Harbin, China.
Shuwei
S
Jia
Institute of Acupuncture, Tianjin Chinese Medical University, Tianjin, China.
Qing
Q
Xia
Department of Neurology of 2nd Affiliated Hospital, Harbin Medical University, Harbin, China.
Benping
B
Zhang
Department of Physiology, Harbin Medical University, Harbin, China. Electronic address: wangling6004@163.com.
Ling
L
Wang
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D004195:Disease Models, Animal; D016291:Dizocilpine Maleate / Q000627:therapeutic use; D004562:Electrocardiography; D005786:Gene Expression Regulation / Q000187:drug effects; D018698:Glutamic Acid / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D020244:Infarction, Middle Cerebral Artery / Q000150:complications*; D007276:Injections, Intraventricular; D008297:Male; D009422:Nervous System Diseases / Q000188:drug therapy / Q000209:etiology; D018696:Neuroprotective Agents / Q000627:therapeutic use; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D018696:Neuroprotective Agents; D016760:Proto-Oncogene Proteins c-fos; D018698:Glutamic Acid; D016291:Dizocilpine Maleate
Arrhythmia; NMDA receptor; glutamate; ischemic stroke; paraventricular nucleus