Zheng C, Zhang T
College of Life Sciences and Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, 300071 Tianjin, PR China; Center for Learning and Memory, The University of Texas at Austin, Austin, TX, USA.
College of Life Sciences and Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, 300071 Tianjin, PR China.
Neuroscience. 2015 Apr 30;292:170-80. doi: 10.1016/j.neuroscience.2015.01.071. Epub 2015 Feb 12.
It is believed that phase synchronization facilitates neural communication and neural plasticity throughout the hippocampal-cortical network, and further supports cognition and memory. The pathway from the ventral hippocampus to the medial prefrontal cortex (mPFC) is thought to play a significant role in emotional memory processing. Therefore, the information transmission on the pathway was hypothesized to be disrupted in the depressive state, which could be related to its impaired synaptic plasticity. In this study, local field potentials (LFPs) from both ventral CA1 (vCA1) and mPFC were recorded in both normal and chronic unpredictable stress (CUS) model rats under urethane anesthesia. LFPs of all rats were recorded before and after the long-term potentiation (LTP) induced on the vCA1-mPFC pathway in order to figure out the correlation of oscillatory synchronization of LFPs and synaptic plasticity. Our results showed the vCA1-to-mPFC unidirectional phase coupling of the theta rhythm, rather than the power of either region, was significantly enhanced by LTP induction, with less enhancement in the CUS model rats compared to that in the normal rats. In addition, theta phase coupling was positively correlated with synaptic plasticity on vCA1-mPFC pathway. Moreover, the theta-slow gamma phase-amplitude coupling in vCA1 was long-term enhanced after high frequency stimulation. These results suggest that the impaired synaptic plasticity in vCA1-mPFC pathway could be reflected by the attenuated theta phase coupling and theta-gamma cross frequency coupling of LFPs in the depression state.
人们认为，相位同步有助于整个海马 - 皮质网络中的神经通信和神经可塑性，并进一步支持认知和记忆。从腹侧海马到内侧前额叶皮质（mPFC）的通路被认为在情绪记忆处理中起重要作用。因此，有人推测该通路上的信息传递在抑郁状态下会受到干扰，这可能与其受损的突触可塑性有关。在本研究中，在乌拉坦麻醉下，记录了正常和慢性不可预测应激（CUS）模型大鼠腹侧CA1（vCA1）和mPFC的局部场电位（LFP）。记录所有大鼠在vCA1 - mPFC通路上诱导长时程增强（LTP）前后的LFP，以弄清楚LFP振荡同步与突触可塑性之间的相关性。我们的结果表明，LTP诱导显著增强了θ节律的vCA1到mPFC单向相位耦合，而不是任何一个区域的功率，与正常大鼠相比，CUS模型大鼠的增强较少。此外，θ相位耦合与vCA1 - mPFC通路上的突触可塑性呈正相关。此外，高频刺激后vCA1中的θ - 慢γ相位 - 振幅耦合长期增强。这些结果表明，抑郁状态下vCA1 - mPFC通路中受损的突触可塑性可能通过LFP的θ相位耦合减弱和θ - γ交叉频率耦合来反映。
