Spriggs M J, Cadwallader C J, Hamm J P, Tippett L J, Kirk I J
School of Psychology, The University of Auckland, New Zealand; Centre for Brain Research, The University of Auckland, New Zealand; Brain Research New Zealand.
School of Psychology, The University of Auckland, New Zealand; Centre for Brain Research, The University of Auckland, New Zealand.
Brain Res Bull. 2017 Apr;130:53-59. doi: 10.1016/j.brainresbull.2016.12.015. Epub 2016 Dec 30.
Age-related changes in neuroplasticity may be central to the cognitive decline associated with healthy ageing. Modulated Long-Term Potentiation (LTP) and Long-Term Depression (LTD) have been repeatedly demonstrated in aged rodents, however the translation to human research has been limited by a scarcity of non-invasive methods for doing so. We have previously demonstrated that, following a block of high frequency presentations of a visual stimulus (referred to as a "visual tetanus"), there is a LTP-like enhancement of the N1b component of the visually evoked potential (VEP) to subsequent low frequency presentations of the same stimulus. The aims of the current study were, firstly, to use this electroencephalography (EEG) paradigm to assess age group differences in neocortical plasticity in humans, and secondly, to expand on the visual LTP paradigm by examining plasticity in another component of the VEP; the P2a. While a young participant group (N=29, age range=19-35) demonstrated the expected LTP-like enhancement of the N1b immediately following the visual tetanus, an older participant group (N=19, age range=68-91) did not. However, both age groups demonstrated a positive shift of the P2a component after repeated presentations of low frequency baseline blocks, which is hypothesized to be an LTD-like shift in the VEP. These results support the rodent literature indicating an age-related shift in threshold for LTP, but a relative preservation of the threshold for LTD. This study not only provides valuable insight into healthy age-related alterations in neocortical plasticity, but is also the first to identify an LTD-like modulation of the VEP in humans.
与年龄相关的神经可塑性变化可能是健康衰老相关认知衰退的核心。在老年啮齿动物中反复证明了调制长时程增强（LTP）和长时程抑制（LTD），然而向人类研究的转化受到缺乏非侵入性方法的限制。我们之前已经证明，在对视觉刺激进行高频呈现（称为“视觉强直刺激”）阻断后，对同一刺激随后的低频呈现，视觉诱发电位（VEP）的N1b成分会出现类似LTP的增强。本研究的目的，首先是使用这种脑电图（EEG）范式评估人类新皮质可塑性的年龄组差异，其次是通过检查VEP的另一个成分P2a的可塑性来扩展视觉LTP范式。虽然年轻参与者组（N = 29，年龄范围 = 19 - 35岁）在视觉强直刺激后立即表现出预期的N1b类似LTP的增强，但老年参与者组（N = 19，年龄范围 = 68 - 91岁）没有。然而，两个年龄组在低频基线块重复呈现后均表现出P2a成分的正向偏移，这被假设为VEP中类似LTD的偏移。这些结果支持了啮齿动物文献，表明LTP阈值存在与年龄相关的偏移，但LTD阈值相对保持不变。本研究不仅为新皮质可塑性中与年龄相关的健康变化提供了有价值的见解，也是首次在人类中识别出VEP的类似LTD的调制。
