Zhang Yujiao, Ahmed Sanya, Neagu Georgiana, Wang Yali, Li Zhenyi, Wen Jianbin, Liu Chunjie, Vreugdenhil Martin
Department of Psychology, Xinxiang Medical University, Jinsui Avenue, Xinxiang, 453003, PR China.
Department of Neuroscience, College of Medical and Dental Sciences, University of Birmingham, Vincent Drive, Birmingham, B15 2TT, United Kingdom.
IBRO Rep. 2019 Jan 8;6:122-131. doi: 10.1016/j.ibror.2019.01.004. eCollection 2019 Jun.
In the intact brain, hippocampal area CA1 alternates between low-frequency gamma oscillations (γ), phase-locked to low-frequency γ in CA3, and high-frequency γ, phase-locked to γ in the medial entorhinal cortex. In hippocampal slices, γ in CA1 is phase-locked to CA3 low-frequency γ. However, when Schaffer collaterals are cut, CA1 can generate its own high-frequency γ. Here we test whether (un)coupling of CA1 γ from CA3 γ can be caused by μ-opioid receptor (MOR) modulation. In CA1 minislices isolated from rat ventral hippocampus slices, MOR activation by DAMGO reduced the dominant frequency of intrinsic fast γ, induced by carbachol. In intact slices, DAMGO strongly reduced the dominant frequency of CA3 slow γ, but did not affect γ power consistently. DAMGO suppressed the phase coupling of CA1 γ to CA3 slow γ and increased the power of CA1 intrinsic fast γ, but not in the presence of the MOR antagonist CTAP. The benzodiazepine zolpidem and local application of DAMGO to CA3 both mimicked the reduction in dominant frequency of CA3 slow γ, but did not reduce the phase coupling. Local application of DAMGO to CA1 reduced phase coupling. These results suggest that MOR-expressing CA1 interneurons, feed-forwardly activated by Schaffer collaterals, are responsible for the phase coupling between CA3 γ and CA1 γ. Modulating their activity may switch the CA1 network between low-frequency γ and high-frequency γ, controlling the information flow between CA1 and CA3 or medial entorhinal cortex respectively.
在完整大脑中，海马体CA1区在低频γ振荡（γ）和高频γ之间交替，低频γ与CA3区的低频γ锁相，高频γ与内嗅皮质的γ锁相。在海马体切片中，CA1区的γ与CA3区的低频γ锁相。然而，当切断海马体联合纤维时，CA1区能够产生自身的高频γ。在此，我们测试CA1区γ与CA3区γ的（非）耦合是否由μ-阿片受体（MOR）调节引起。在从大鼠腹侧海马体切片分离的CA1微小切片中，DAMGO激活MOR降低了由卡巴胆碱诱导的固有快速γ的主导频率。在完整切片中，DAMGO强烈降低了CA3区慢γ的主导频率，但并未持续影响γ功率。DAMGO抑制了CA1区γ与CA3区慢γ的相位耦合，并增加了CA1区固有快速γ的功率，但在存在MOR拮抗剂CTAP时则不会。苯二氮䓬类药物唑吡坦以及将DAMGO局部应用于CA3区均模拟了CA3区慢γ主导频率的降低，但并未减少相位耦合。将DAMGO局部应用于CA1区可减少相位耦合。这些结果表明，表达MOR的CA1中间神经元由海马体联合纤维前馈激活，负责CA3区γ与CA1区γ之间的相位耦合。调节它们的活动可能会使CA1网络在低频γ和高频γ之间切换，分别控制CA1区与CA3区或内嗅皮质之间的信息流。
