Kole M H P, Costoli T, Koolhaas J M, Fuchs E
Clinical Neurobiology Laboratory, German Primate Center, Goettingen, Germany.
Neuroscience. 2004;125(2):337-47. doi: 10.1016/j.neuroscience.2004.02.014.
The negative impact of chronic stress at the structure of apical dendrite branches of cornu ammonis 3 (CA3) pyramidal neurons is well established. However, there is no information available on the CA3 dendritic organization related to short-lasting stress, which suffices to produce long-term habituation or sensitization of anxiety behaviors and neuroendocrine responses. Here, we tested the effects evoked by brief stress on the arrangements of CA3 pyramidal neuron dendrites, and the activity-dependent properties of the commissural-associational (C/A) excitatory postsynaptic potentials (EPSPs). Adult male rats were socially defeated followed by 3 weeks without further treatment or as comparison exposed to a regimen of a social defeat every second day for the same time period. We assessed CA3 pyramidal neurons with somatic whole-cell recording and neurobiotin application in acute hippocampal slices. The results from morphometric analysis of post hoc reconstructions demonstrated that CA3 dendrites from repeatedly stressed rats were reduced in surface area and length selectively at the apical cone (70% of control, approximately 280 microm from the soma). Brief stress, however, produced a similar decrease in apical dendritic length (77% of control, approximately 400 microm from the soma), accompanied by an increased length (167% of control) and branch complexity at the basal cone. The structural changes of the dendrites significantly influenced signal propagation by shortening the onset latency of EPSPs and increasing input resistance (r=0.45, P<0.01), of which the first was significantly changed in repeatedly stressed animals. Both brief and repeated stress long-lastingly impaired long-term potentiation of C/A synapses to a similar degree (P<0.05). These data indicate that the geometric plasticity of CA3 dendrites is dissociated from repetition of aversive experiences. A double social conflict suffices to drive a dynamic reorganization, by site-selective elimination and de novo growth of dendrite branches over the course of weeks after the actual experience.
慢性应激对海马角3（CA3）锥体神经元顶端树突分支结构的负面影响已得到充分证实。然而，关于与短期应激相关的CA3树突组织尚无可用信息，短期应激足以产生焦虑行为和神经内分泌反应的长期习惯化或敏感化。在此，我们测试了短暂应激对CA3锥体神经元树突排列以及联合-联络（C/A）兴奋性突触后电位（EPSP）的活动依赖性特性所引发的影响。成年雄性大鼠遭受社会挫败，随后3周不再接受进一步处理，或者作为对照，在相同时间段内每隔一天接受一次社会挫败方案处理。我们在急性海马切片中采用体细胞全细胞记录和神经生物素应用来评估CA3锥体神经元。事后重建的形态计量学分析结果表明，反复应激大鼠的CA3树突在顶端锥体处的表面积和长度选择性减少（为对照组的70%，距胞体约280微米）。然而，短暂应激使顶端树突长度出现类似程度的减少（为对照组的77%，距胞体约400微米），同时伴随着基部锥体处长度增加（为对照组的167%）以及分支复杂性增加。树突的结构变化通过缩短EPSP的起始潜伏期和增加输入电阻，显著影响信号传播（r = 0.45，P < 0.01），其中前者在反复应激的动物中显著改变。短暂应激和反复应激均长期且同等程度地损害C/A突触的长期增强（P < 0.05）。这些数据表明，CA3树突的几何可塑性与厌恶经历的重复无关。一次双重社会冲突足以驱动动态重组，即在实际经历后的数周内通过树突分支的位点选择性消除和新生生长来实现。
