摘要
目的探究胰高血糖素样肽-1(GLP-1)受体激动剂Exendin-4及内源性GLP-1对海马CA3区神经元自发放电的调控作用。方法利用在体细胞外单细胞电生理记录方法,观察三管微电极微压力注射10μmol/L Exendin-4和10μmol/L Exendin-9-39(GLP-1受体阻断剂)对大鼠海马CA3区神经元自发放电频率的影响。结果在记录到的22个海马CA3区神经元中,Exendin-4使17个神经元放电频率显著增高(t=6.286,P<0.01),平均升高(149.67±18.94)%,与生理盐水组相比差异有显著性(Z=3.571,P<0.01)。在记录到的14个海马CA3区神经元中,Exendin-9-39使10个神经元放电频率显著降低(t=7.968,P<0.01),平均降低(61.90±6.10)%,与生理盐水组相比差异有显著性(Z=3.145,P<0.01)。结论Exendin-4兴奋海马CA3区神经元,内源性GLP-1参与调节海马CA3区神经元自发放电。
Objective To investigate the role of the glucagon-like peptide 1(GLP-1)receptor agonist Exendin-4 and endogenous GLP-1 in regulating spontaneous discharge of neurons in the hippocampal CA3 region.Methods In vivo extracellular single-unit recordings were used to observe the effect of three-barrel glass micro-electrode micro-pressure injection of 10μmol/L Exendin-4 versus 10μmol/L Exendin-9-39(a GLP-1 receptor antagonist)on the spontaneous discharge frequency of neurons in the hippocampal CA3 region.Results Among the 22 neurons recorded in the hippocampal CA3 region,17 showed a significant increase in spontaneous discharge frequency caused by Exendin-4(t=6.286,P<0.01),with a mean increase of 149.67%±18.94%,which was significantly different from that in the saline group(Z=3.571,P<0.01).Among the 14 neurons recorded in the hip-pocampal CA3 region,10 showed a significant reduction in spontaneous discharge frequency caused by Exendin-9-39(t=7.968,P<0.01),with a mean reduction of(61.90±6.10)%,which was significantly different from that in the saline group(Z=3.145,P<0.01).Conclusion Exendin-4 can excite neurons in the hippocampal CA3 region,and endogenous GLP-1 is involved in regulating the spontaneous discharge of neurons in the hippocampal CA3 region.
作者
孙慧哲
刘翠
沈方帅
陈心怡
薛雁
陈蕾
SUN Huizhe;LIU Cui;SHEN Fangshuai;CHEN Xinyi;XUE Yan;CHEN Lei(Department of Physiology and Pathophysiology,School of Basic Medicine,Qingdao University Medical College,Qingdao 266071,China)
出处
《青岛大学学报(医学版)》
CAS
2023年第3期353-356,共4页
Journal of Qingdao University(Medical Sciences)
基金
国家自然科学基金资助项目(32200939)
山东省自然科学基金资助项目(ZR2022QC225)。