SIP30 in the ventrolateral orbital cortex contributes to affective pain in rat
作者单位：Institutes of Brain Science and State Key Laboratory of Medical Neurobiology Fudan University
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：1006[医学-中西医结合] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学]
关 键 词：ventrolateral orbital cortex neuropathic pain affective pain SIP30
摘 要：Objective SIP30（SNAP25 interacting protein of 30）, interacting with SNAP25, is widely expressed in the mammal brain and plays a role in neural activities. Our previous studies demonstrated that SIP30 in the r ACC mediates neuropathic pain-evoked negative emotion via modulation of glutamate release and excitatory synaptic transmission. Here, using a chronic constriction injury（CCI） model of neuropathic pain, we aim to explore the role of SIP30 in the ventrolateral orbital cortex（VLO） in painrelated negative emotion. Methods Rats were performed in a chamber with one half painted white（light area） and the other half painted black（dark area）, and measured neuropathic pain-evoked place escape/avoidance paradigm（PEAP） to quantify the level of negative emotion evoked by painful stimuli using a von Frey hair. Results Bilateral excitotoxic（quinolinic acid 200 nmol/ml） lesions of the VLO significantly blocked the formation of pain-related emotion without influence on CCI-induced mechanical allodynia and heat hyperalgesia. CCI induced a bilateral increase of SIP30 in the VLO. Upregulated SIP30 is predominantly colocalized with Neu N, a neuronal marker, but not with GFAP, an astrocyte marker, or OX-42, a microglial marker. Inhibition of CCImediated induction of SIP30 by intra-VLO injection of sh RNA targeting the rat sip30 gene reduced affective pain in the PEAP test. Interestingly, knockdown of SIP30 did not affect CCI-induced evoked pain hyperalgesia. Neither did it affect general learning and memory. Conclusion The present study strongly suggests that SIP30 in the ventrolateral orbital cortex plays an important role in neuropathic pain-evoked aversion.