Vorobyov Vasily, Deev Alexander, Chaprov Kirill, Ninkina Natalia
Institute of Cell Biophysics, Russian Academy of Sciences, 142290 Pushchino, Russia.
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, 142290 Pushchino, Russia.
Biomedicines. 2024 Apr 16;12(4):881. doi: 10.3390/biomedicines12040881.
The malfunctioning of the brain synucleins is associated with pathogenesis of Parkinson's disease. Synucleins' ability to modulate various pre-synaptic processes suggests their modifying effects on the electroencephalogram (EEG) recorded from different brain structures. Disturbances in interrelations between them are critical for the onset and evolution of neurodegenerative diseases. Recently, we have shown that, in mice lacking several synucleins, differences between the frequency spectra of EEG from different brain structures are correlated with specificity of synucleins' combinations. Given that EEG spectra are indirect characteristics of inter-structural relations, in this study, we analyzed a coherence of instantaneous values for EEGs recorded from different structures as a direct measure of "functional connectivity" between them.
EEG data from seven groups of knock-out (KO) mice with combined deletions of alpha, beta, and gamma synucleins versus a group of wild-type (WT) mice were compared. EEG coherence was estimated between the cortex (MC), putamen (Pt), ventral tegmental area (VTA), and substantia nigra (SN) in all combinations.
EEG coherence suppression, predominantly in the beta frequency band, was observed in KO mice versus WT littermates. The suppression was minimal in MC-Pt and VTA-SN interrelations in all KO groups and in all inter-structural relations in mice lacking either all synucleins or only beta synuclein. In other combinations of deleted synucleins, significant EEG coherence suppression in KO mice was dominant in relations with VTA and SN.
Deletions of the synucleins produced significant attenuation of intra-cerebral EEG coherence depending on the imbalance of different types of synucleins.
脑突触核蛋白功能异常与帕金森病的发病机制相关。突触核蛋白调节各种突触前过程的能力表明它们对从不同脑结构记录的脑电图（EEG）有修饰作用。它们之间相互关系的紊乱对神经退行性疾病的发生和发展至关重要。最近，我们发现，在缺乏几种突触核蛋白的小鼠中，不同脑结构的脑电图频谱差异与突触核蛋白组合的特异性相关。鉴于脑电图频谱是结构间关系的间接特征，在本研究中，我们分析了从不同结构记录的脑电图瞬时值的相干性，作为它们之间“功能连接性”的直接测量指标。
比较了七组α、β和γ突触核蛋白联合缺失的基因敲除（KO）小鼠与一组野生型（WT）小鼠的脑电图数据。对所有组合中的皮质（MC）、壳核（Pt）、腹侧被盖区（VTA）和黑质（SN）之间的脑电图相干性进行了评估。
与野生型同窝小鼠相比，基因敲除小鼠中观察到脑电图相干性抑制，主要在β频段。在所有基因敲除组中，MC-Pt和VTA-SN相互关系以及在缺乏所有突触核蛋白或仅缺乏β突触核蛋白的小鼠的所有结构间关系中，抑制作用最小。在其他缺失突触核蛋白的组合中，基因敲除小鼠中显著的脑电图相干性抑制在与VTA和SN的关系中占主导地位。
突触核蛋白的缺失导致脑内脑电图相干性显著减弱，这取决于不同类型突触核蛋白的失衡。
