BACKGROUND:The insular cortex and habenular nucleus may be a regulatory center for obstructive sleep apnea syndrome,and dyspnea may be caused by insular cortex activity.The insular cortex is a cortical representation of obstructive sleep apnea syndrome.The habenular nucleus is a station for descending insular cortex activity.OBJECTIVE:Through actively stimulating the rat insular cortex,to observe rat respiratory movement,myoelectric activities of genioglossus,arterial partial pressure of oxygen,partial pressure of carbon dioxide and acidity-alkalinity,and to verify a hypothesis that the insular cortex is a superior-position regulation center,and the habenular nucleus is an inferior-position nervous nuclei of the insular cortex in patients with obstructive sleep apnea syndrome.DESIGN,TIME AND SETTING:The randomized,controlled animal study was performed at the Laboratory of Electrophysiology,Department of Physiology,Norman Bathune College of Medicine,Jilin University,China from September 2004 to June 2008.MATERIALS:We used L-glutamic acid(Dingguo Biological Product Research Center,Beijing,China),lidocaine hydrochloride(Seventh Pharmacy Co.,Ltd.,Wuxi,China),electric stimulator(Nihon Kohden,Japan),and an AVL-OPTI blood gas analyzer(AVL Scientific Co.,Roswell,GA,USA).METHODS:The insular cortex of healthy adult Wistar rats underwent electrostimulation and L-glutamic acid stimulation to record changes in the myoelectric activity of genioglossus and respiratory movement.Some rats were injected with lidocaine to block the habenular nucleus before electrostimulation or L-glutamic acid stimulation.L-glutamic acid and lidocaine were injected by microelectrodes embedded in nuclear groups.MAIN OUTCOME MEASURES:Myoelectric activities of genioglossus,arterial partial pressure of oxygen,partial pressure of carbon dioxide and acidity-alkalinity were measured following apnea in rats undergoing electrostimulation in the insular cortex and following blockade of the habenular nucleus.RESULTS:Following electrostimulation and L-glutamic acid stimulation,rats developed apnea or respiratory rhythm disorders.Simultaneously,the amplitude of myoelectric activity of the genioglossus was reduced(P < 0.01),and the electromyogram integral was decreased(P < 0.01).Arterial blood gas analysis showed arterial blood acidosis,a decrease in pH(P < 0.05),and an increase in the negative value of alkaline reserve(P < 0.01).Lidocaine in the habenular nuclear blocked respiratory and other index changes after insular cortex stimulation.CONCLUSION:Dyspnea induced by stimulating the insular cortex may require the habenular nucleus.Paralysis of the habenular nucleus can completely eliminate insular cortex stimulation-induced dyspnea. BACKGROUND: The insular cortex and habenular nucleus may be a regulatory center for obstructive sleep apnea syndrome, and dyspnea may be caused by insular cortex activity. The insular cortex is a cortical representation of obstructive sleep apnea syndrome. Habenular nucleus is a station for descending insular cortex activity. OBJECTIVE: Through actively stimulating the rat insular cortex, to observe rat respiratory movement, myoelectric activities of genioglossus, arterial partial pressure of oxygen, partial pressure of carbon dioxide and acidity-alkalinity, and to verify a hypothesis that the insular cortex is a superior-position regulation center, and the habenular nucleus is an inferior-position nervous nuclei of the insular cortex in patients with obstructive sleep apnea syndrome. DESIGN, TIME AND SETTING: The randomized, controlled animal study was performed at the Laboratory of Electrophysiology , Department of Physiology, Norman Bathune College of Medicine, Jilin University, China from September 2004 to June 2008. MAIALIALS: We used L-glutamic acid (Dingguo Biological Product Research Center, Beijing, China), lidocaine hydrochloride (Seventh Pharmacy Co., Ltd., Wuxi, China), electric stimulator (Nihon Kohden, Japan) and AVL-OPTI blood gas analyzer (AVL Scientific Co., Roswell, GA, USA). METHODS: The insular cortex of healthy adult Wistar rats underwent electrostimulation and L-glutamic acid stimulation to record changes in the myoelectric activity of genioglossus and respiratory movement.Some rats were injected with lidocaine to block the habenular nucleus before electrostimulation or L-glutamic acid stimulation. L-glutamic acid and lidocaine were injected by microelectrodes embedded in nuclear groups. MAIN OUTCOME MEASURES: Myoelectric activities of genioglossus, arterial partial pressure of oxygen, partial pressure of carbon dioxide and acidity-alkalinity were measured following apnea in rats undergoing electrostimulation in the insular cortex and following blockade of the habenular nucleus. RESULTS: Following electrostimulation and L-glutamic acid stimulation, rats developed apnea or respiratory rhythm disorders. Simultaneously, the amplitude of myoelectric activity of the genioglossus was reduced (P <0.01), and the electromyogram integral was decreased (P <0.01) Blood gas analysis showed arterial blood acidosis, a decrease in pH (P <0.05), and an increase in the negative value of alkaline reserve (P <0.01) .Lidocaine in the habenular nuclear blocked respiratory and other index changes after insular cortex stimulation. CONCLUSION: Dyspnea induced by stimulating the insular cortex may require the habenular nucleus. Paralysis of the habenular nucleus can completely eliminate insular cortex stimulation-induced dyspnea.