Carson Richard G, Kennedy Niamh C
Trinity College Institute of Neuroscience and School of Psychology, Trinity College Dublin Dublin, Ireland ; School of Psychology, Queen's University Belfast Belfast, UK.
School of Psychology, Queen's University Belfast Belfast, UK ; School of Rehabilitation Sciences University of East Anglia Norwich, UK.
Front Hum Neurosci. 2013 Dec 3;7:823. doi: 10.3389/fnhum.2013.00823.
Paired Associative Stimulation (PAS) has come to prominence as a potential therapeutic intervention for the treatment of brain injury/disease, and as an experimental method with which to investigate Hebbian principles of neural plasticity in humans. Prototypically, a single electrical stimulus is directed to a peripheral nerve in advance of transcranial magnetic stimulation (TMS) delivered to the contralateral primary motor cortex (M1). Repeated pairing of the stimuli (i.e., association) over an extended period may increase or decrease the excitability of corticospinal projections from M1, in manner that depends on the interstimulus interval (ISI). It has been suggested that these effects represent a form of associative long-term potentiation (LTP) and depression (LTD) that bears resemblance to spike-timing dependent plasticity (STDP) as it has been elaborated in animal models. With a large body of empirical evidence having emerged since the cardinal features of PAS were first described, and in light of the variations from the original protocols that have been implemented, it is opportune to consider whether the phenomenology of PAS remains consistent with the characteristic features that were initially disclosed. This assessment necessarily has bearing upon interpretation of the effects of PAS in relation to the specific cellular pathways that are putatively engaged, including those that adhere to the rules of STDP. The balance of evidence suggests that the mechanisms that contribute to the LTP- and LTD-type responses to PAS differ depending on the precise nature of the induction protocol that is used. In addition to emphasizing the requirement for additional explanatory models, in the present analysis we highlight the key features of the PAS phenomenology that require interpretation.
配对联想刺激（PAS）已成为一种潜在的治疗脑损伤/疾病的治疗性干预手段，并作为一种用于研究人类神经可塑性的赫布原理的实验方法而备受关注。典型地，在经颅磁刺激（TMS）施加到对侧初级运动皮层（M1）之前，先将单个电刺激施加到外周神经。在较长时间内重复刺激配对（即联想）可能会增加或降低M1皮质脊髓投射的兴奋性，其方式取决于刺激间隔（ISI）。有人认为，这些效应代表了一种联想性长时程增强（LTP）和长时程抑制（LTD）的形式，类似于在动物模型中阐述的尖峰时间依赖性可塑性（STDP）。自从首次描述PAS的主要特征以来，已经出现了大量的经验证据，并且鉴于已经实施的与原始方案的差异，现在是时候考虑PAS的现象学是否仍然与最初揭示的特征一致了。这种评估必然与解释PAS与假定参与的特定细胞途径相关的效应有关，包括那些遵循STDP规则的途径。证据的平衡表明，导致对PAS产生LTP型和LTD型反应的机制因所使用的诱导方案的确切性质而异。除了强调需要额外的解释模型之外，在本分析中，我们突出了需要解释的PAS现象学的关键特征。
