Xu Xiaxia, Zheng Chenguang, An Lei, Wang Rubin, Zhang Tao
College of Life Sciences and Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, Tianjin, 300071, People's Republic of China.
Center for Learning and Memory, The University of Texas at Austin, Austin, TX, USA.
Brain Topogr. 2016 Jul;29(4):539-51. doi: 10.1007/s10548-016-0485-3. Epub 2016 Mar 11.
Theta and gamma oscillations are believed to play an important role in cognition and memory, and their phase coupling facilitates the information transmission in hippocampal-cortex network. In a rat model of chronic stress, the phase coupling of both theta and gamma oscillations between ventral hippocampal CA1 (vCA1) and medial prefrontal cortex (mPFC) was found to be disrupted, which was associated with the impaired synaptic plasticity in the pathway. However, little was known about the mechanisms underlying the process. In order to address this issue, both dopamine and serotonin as monoaminergic neurotransmitters were involved in this study, since they were crucial factors in pathological basis of depressive disorder. Local field potentials (LFPs) were recorded simultaneously at both vCA1 and mPFC regions under anesthesia, before and after the injection of dopamine D1 receptor antagonist and 5-HT1A receptor agonist, respectively. The results showed that the blockage of D1 receptor could lead to depression-like decrement on theta phase coupling. In addition, the activation of 5-HT1A receptor enhanced vCA1-mPFC coupling on gamma oscillations, and attenuated CA1 theta-fast gamma cross frequency coupling. These data suggest that the theta phase coupling between vCA1 and mPFC may be modulated by dopamine system that is an underlying mechanism of the cognitive dysfunction in depression. Besides, the serotonergic system is probably involved in the regulation of gamma oscillations coupling in vCA1-mPFC network.
θ波和γ波振荡被认为在认知和记忆中发挥重要作用，并且它们的相位耦合促进了海马-皮质网络中的信息传递。在慢性应激大鼠模型中，发现腹侧海马CA1区（vCA1）和内侧前额叶皮质（mPFC）之间的θ波和γ波振荡的相位耦合被破坏，这与该通路中突触可塑性受损有关。然而，对于这一过程的潜在机制知之甚少。为了解决这个问题，本研究涉及多巴胺和5-羟色胺这两种单胺能神经递质，因为它们是抑郁症病理基础中的关键因素。在麻醉状态下，分别在注射多巴胺D1受体拮抗剂和5-HT1A受体激动剂之前和之后，同时记录vCA1和mPFC区域的局部场电位（LFP）。结果表明，D1受体的阻断可导致θ波相位耦合出现类似抑郁的下降。此外，5-HT1A受体的激活增强了vCA1-mPFC在γ波振荡上的耦合，并减弱了CA1区θ波-快速γ波交叉频率耦合。这些数据表明，vCA1和mPFC之间的θ波相位耦合可能受多巴胺系统调节，这是抑郁症认知功能障碍的潜在机制。此外，5-羟色胺能系统可能参与调节vCA1-mPFC网络中的γ波振荡耦合。
