Zhang Li, Li Yan-Hai, Meng Kai, Han Tai-Zhen
Department of Physiology, School of Medicine, Xi'an Jiaotong University, Zhuque Dajie 205, Xi'an, 710061, P.R. China.
Chin J Physiol. 2010 Oct 31;53(5):328-36. doi: 10.4077/cjp.2010.amk054.
Activity-dependent structural plasticity of dendritic spines of pyramidal neurons in the central neuron system has been proposed to be a cellular basis of learning and memory. Long-term potentiation (LTP) is accompanied by changes in synaptic morphology and structural remodeling of dendritic spines. However, there is considerable uncertainty as to the nature of the adjustment. The present study tested whether immunoreactive phospho-cofilin, an index of altered actin filament assembly, could be increased by theta-burst stimulations (TBS), which is an effective stimulation pattern for inducing LTP in the hippocampus. The slope of fEPSPs evoked by TBS to Schaffer collateral-commissural fibers in hippocampal slices was measured, and p-cofilin expression was examined using immunofluorescence techniques. Results indicated that saturated L-LTP was produced by multiple TBS episodes to Schaffer collateral-commissural fibers in the hippocampal CA1 area, and TBSs also increased immunoreactive p-cofilin expression in the stratum radiatum of the hippocampal CA1 area and pyramidal layer of the subiculum. D-2-amino-5-phosphonovalerate (D-APV) prevented LTP and expression of p-cofilin immunoreactive induced by multiple TBS episodes in the stratum radiatum of the hippocampal CA1 area. Two paired-pulse low-frequency stimulation (PP-LFS) episodes to Schaffer collateral-commissural fibers induced long-term depression (LTD), and did not affect p-cofilin expression in the stratum radiatum of the hippocampal CA1 area. These results suggest that LTP induction is associated with altered actin filament assembly. Moreover, the CA1 and subiculum areas of the hippocampal formation possibly cooperate with each other in important physiological functions, such as learning and memory, or in pathological diseases, such as epilepsy.
中枢神经系统中锥体神经元树突棘的活动依赖性结构可塑性被认为是学习和记忆的细胞基础。长时程增强(LTP)伴随着突触形态的变化和树突棘的结构重塑。然而,关于这种调节的本质存在相当大的不确定性。本研究测试了免疫反应性磷酸化丝切蛋白(一种肌动蛋白丝组装改变的指标)是否能通过θ波爆发刺激(TBS)增加,TBS是在海马体中诱导LTP的有效刺激模式。测量了TBS诱发海马切片中Schaffer侧支-连合纤维的场兴奋性突触后电位(fEPSP)斜率,并使用免疫荧光技术检测了磷酸化丝切蛋白的表达。结果表明,多次TBS刺激海马CA1区的Schaffer侧支-连合纤维可产生饱和的L-LTP,TBS还增加了海马CA1区辐射层和下托锥体层中免疫反应性磷酸化丝切蛋白的表达。D-2-氨基-5-磷酸戊酸(D-APV)可阻止海马CA1区辐射层中多次TBS刺激诱导的LTP和磷酸化丝切蛋白免疫反应性的表达。对Schaffer侧支-连合纤维进行两次配对脉冲低频刺激(PP-LFS)可诱导长时程抑制(LTD),且不影响海马CA1区辐射层中磷酸化丝切蛋白的表达。这些结果表明,LTP的诱导与肌动蛋白丝组装的改变有关。此外,海马结构的CA1区和下托区可能在学习和记忆等重要生理功能或癫痫等病理疾病中相互协作。
Front Aging Neurosci. 2017-8-31