Hua-Xing Si, Xiao-Die Liu, Chao-Yi Sun, Shan-Ming Yang, Han Zhao, Xian-Xia Yan, Tao Chen, Pan Wang
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引用次数: 0
Abstract
Neuropathic pain (NP) is a severe disease caused by a primary disease or lesion affecting the somatosensory nervous system. It is reported that NP is related to the increased activity of glutamatergic pyramidal cells and changed neural oscillations in the anterior cingulate cortex (ACC). Arginine vasopressin (AVP), a neurohypophyseal hormone, has been shown to cause pain-alleviating effects when applied to the peripheral system. However, the extent to which, and the mechanisms by which, AVP induces analgesic effects in the central nervous system remains unclear. In the present study, we observed that intranasal delivery of AVP inhibited mechanical pain, thermal pain, and spontaneous pain sensitivity in mice with spared nerve injury. Meanwhile, AVP application exclusively reduced the FOS expression in the pyramidal cells but not interneurons in the ACC. In vivo electrophysiological recording of the ACC further showed that AVP application not only inhibited the theta oscillation in local field potential analysis but also reduced the firing rate of spikes of pyramidal cells in the ACC in neuropathic pain mice. In summary, AVP induces analgesic effects by inhibiting neural theta oscillations and the spiking of pyramidal cells of the ACC in mice with neuropathic pain, which should provide new potential noninvasive methods for clinical treatment of chronic pain.NEW & NOTEWORTHY Following intranasal administration of arginine vasopressin (AVP), the pain thresholds for mechanical and thermal nociception significantly increased in the spared nerve injury (SNI) group; exogenous intranasal delivery of AVP improved the physical coordination of SNI mice, resulting in an analgesic effect; AVP treatment significantly reduced the increased firing rate of PYRACC of the SNI group; AVP treatment significantly inhibited the elevated theta oscillation in the anterior cingulate cortex (ACC) in SNI mice.
期刊介绍:
The American Journal of Physiology-Endocrinology and Metabolism publishes original, mechanistic studies on the physiology of endocrine and metabolic systems. Physiological, cellular, and molecular studies in whole animals or humans will be considered. Specific themes include, but are not limited to, mechanisms of hormone and growth factor action; hormonal and nutritional regulation of metabolism, inflammation, microbiome and energy balance; integrative organ cross talk; paracrine and autocrine control of endocrine cells; function and activation of hormone receptors; endocrine or metabolic control of channels, transporters, and membrane function; temporal analysis of hormone secretion and metabolism; and mathematical/kinetic modeling of metabolism. Novel molecular, immunological, or biophysical studies of hormone action are also welcome.