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Arginine Vasopressin Effects on Membrane Potentials of Preop...

Arginine Vasopressin Effects on Membrane Potentials of Preoptic Area Temperature-Sensitive and-Insensitive Neurons in Rat Hypothalamic Tissue Slices

作     者:Yu Tang Yan-Ni Sun Run Xu Xiao Huang Shuang Gu Cheng-Cheng Hong Mi-Jia Liu Heng Jiang 

作者单位:Key Laboratory of Thermoregulatory and Inflammation of Sichuan Higher Education Institutes Chengdu Medical College Department of Physiology Chengdu Medical College Department of Medical Laboratory Chengdu Medical College Department of Public Health Chengdu Medical College School of Clinical Medicine Chengdu Medical College 

会议名称:《中国神经科学学会第十二届全国学术会议》

会议日期:2017年

学科分类:0710[理学-生物学] 07[理学] 071006[理学-神经生物学] 

基  金:supported by the National Natural Science Foundation of China Grants 30870901 and 31300962 

关 键 词:arginine vasopressin preoptic area(POA) resting potential thermosensitivity 

摘      要:Arginine vasopressin(AVP), which plays a tonic negative regulation role in thermoregulation, is an important endogenous mediator in thermoregulation. Moreover, AVP increased the spontaneous firing activity and firing rate thermosensitivity of warmsensitive neurons while it decreased that in cold-sensitive and temperature-insensitive neurons in the preoptic area(POA) of the hypothalamus. Since POA neurons are important in precise thermoregulatory responses, these results indicate that there is an association between the AVP-induced tonic negative thermoregulation and AVP-induced change in firing activity of POA neurons. The electrophysiological mechanisms through which AVP controls the firing activity of POA neurons, however, remain unclear. Therefore, this investigation used an in vitro hypothalamic brain slice preparation and whole cell recording to examine the membrane potential response of temperaturesensitive and-insensitive neurons in rat POA to bath applications of AVP or V1 a receptor antagonist. By monitoring the neuron’s changes in resting potential and membrane potential thermosensitivity before and during experimental perfusion, we found that AVP increased the change of the resting potential in 50% of temperature-insensitive neurons and reduced it in the others. These changes are owing to the AVP enhancing the thermosensitivity of membrane potential in nearly 50% of temperature-insensitive neurons. For temperature-sensitive neurons, however, AVP changed the resting potential and membrane potential thermosensitivity, but there were no resulting differences between the different neuronal types. In all neurons, there was no correlation between firing rate thermosensitivity and change in membrane potential before and during AVP or V1 a receptor antagonist perfusion. Meanwhile, there was no correlation between firing rate thermosensitivity and membrane potential thermosensitivity in all neurons during experimental perfusion. The present study found no evidence

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