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作 者:祝福存[1] 陈瑜[1] 林春[1] 蔡琴燕 陈爱琴[1]
机构地区:[1]福建医科大学基础医学院神经生物学中心疼痛研究室,福州350004 [2]莆田市第一医院儿科,莆田351100
出 处:《神经解剖学杂志》2012年第2期151-156,共6页Chinese Journal of Neuroanatomy
基 金:福建省自然科学基金(C0910595);福建医科大学重大科研项目基金(09ZD009);福建医科大学博士启动基金(2010BS008)
摘 要:目的:探讨尼氟酸(HCN2特异性阻断剂)对慢性内脏痛大鼠海马CA1(cornu ammonis 1)区突触长时程增强(LTP)的影响。方法:选用新生SD大鼠(雌雄不分)出生后8~14 d内,每天固定时间给予1次60 mmHg压力的结直肠扩张刺激建立慢性内脏痛模型,大鼠成年后通过测量腹外斜肌对结直肠扩张引起的放电反应来评估肠道痛觉的敏感性。采用离体脑片场电位的记录方法,观察慢性内脏痛大鼠海马CA1区场电位LTP的变化,并观察不同浓度(25~75 mg/L)的尼氟酸对慢性内脏痛大鼠海马CA1区场电位LTP的影响。结果:慢性内脏痛大鼠海马基础场电位的幅值及斜率与正常大鼠比较无显著性差异,但高频刺激后模型大鼠诱导出的LTP幅值及斜率的变化率与正常大鼠比较均显著增加(P<0.05);尼氟酸对正常大鼠离体海马场电位LTP的峰值和斜率没有任何影响,但是不同剂量(25~75 mg/L)的尼氟酸可剂量依赖性显著降低慢性内脏痛大鼠离体海马场电位LTP的峰值及斜率。结论:HCN2通道可能参与慢性内脏痛大鼠海马场电位LTP的易化过程。Objective: To investigate the effect of niflumic acid(NFA,the specific HCN2 bloker) on synaptic long term potentiation(LTP) in the hippocampus CA1 region in rats with chronic visceral pain.Methods: Model rats with chronic visceral pain received 60 mmHg colon stimulation(CI) once daily during post neonatal days 8-14.The amplitude of external oblique muscle of abdomen(EOMA) discharge were tested to assess the visceral sensitivity of rats when they were adult.The field potential LTP was observed in control and model rats by the recording of field potential in hippocampal CA1 region in vitro.And the effect of NFA(25-75 mg/L) in different doses on the LTP in hippocampus CA1 region slices were observed in model rats.Results: Compared with control rats,no significant difference was found between the amplitude or slope of the basal synaptic responses in hippocampus slices of the model rats and those of the control rats.However,the amplitude and slope of the field potential LTP that high-frequency stimulation(HFS) induced in model rats were significantly higher than those of the control rats(P〈0.05).NFA had no effects on the amplitude and slope of the field potential LTP in hippocampus of the control rats.However,in model rat,the amplitude and slope of the field potential LTP in hippocampus were all dose-dependently decreased by NFA(25-75 mg/L).Conclusion: HCN2 channel might be involved in the facilitation of LTP in hippocampus of chronic visceral pain.
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