Center for Bioelectronic Medicine, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset NY 11030, USA; Department of Physiology & Biophysics, University of Washington, 1705 NE Pacific St, Seattle, WA 98195, USA.
Department of Physiology & Biophysics, University of Washington, 1705 NE Pacific St, Seattle, WA 98195, USA.
Curr Biol. 2018 Aug 20;28(16):2515-2526.e4. doi: 10.1016/j.cub.2018.07.009. Epub 2018 Aug 9.
The functional role of cortical beta oscillations, if any, remains unresolved. During oscillations, the periodic fluctuation in excitability of entrained cells modulates transmission of neural impulses and periodically enhances synaptic interactions. The extent to which oscillatory episodes affect activity-dependent synaptic plasticity remains to be determined. In nonhuman primates, we delivered single-pulse electrical cortical stimulation to a "stimulated" site in sensorimotor cortex triggered on a specific phase of ongoing beta (12-25 Hz) field potential oscillations recorded at a separate "triggering" site. Corticocortical connectivity from the stimulated to the triggering site as well as to other (non-triggering) sites was assessed by cortically evoked potentials elicited by test stimuli to the stimulated site, delivered outside of oscillatory episodes. In separate experiments, connectivity was assessed by intracellular recordings of evoked excitatory postsynaptic potentials. The conditioning paradigm produced transient (1-2 s long) changes in connectivity between the stimulated and the triggering site that outlasted the duration of the oscillatory episodes. The direction of the plasticity effect depended on the phase from which stimulation was triggered: potentiation in depolarizing phases, depression in hyperpolarizing phases. Plasticity effects were also seen at non-triggering sites that exhibited oscillations synchronized with those at the triggering site. These findings indicate that cortical beta oscillations provide a spatial and temporal substrate for short-term, activity-dependent synaptic plasticity in primate neocortex and may help explain the role of oscillations in attention, learning, and cortical reorganization.
皮质β 振荡的功能作用（如果有的话）仍未解决。在振荡期间，被锁定细胞兴奋性的周期性波动调节神经冲动的传递，并周期性地增强突触相互作用。振荡事件对依赖活动的突触可塑性的影响程度仍有待确定。在非人类灵长类动物中，我们在记录于单独的“触发”部位的正在进行的β（12-25Hz）场电位振荡的特定相位上，对感觉运动皮质中的“刺激”部位施加单次电皮质刺激。通过对刺激部位施加测试刺激来评估从刺激部位到触发部位以及到其他（非触发）部位的皮质间连接，皮质诱发电位被记录下来。在单独的实验中，通过对诱发兴奋性突触后电位的细胞内记录来评估连接性。该条件作用范式在刺激部位和触发部位之间产生了短暂的（1-2 秒长）连接性变化，其持续时间超过了振荡的持续时间。塑性效应的方向取决于刺激触发的相位：去极化相增强，超极化相抑制。在与触发部位同步振荡的非触发部位也观察到了可塑性效应。这些发现表明，皮质β 振荡为灵长类新皮质中的短期、依赖活动的突触可塑性提供了一个空间和时间基础，并可能有助于解释振荡在注意力、学习和皮质重组中的作用。
