Murphy Kathryn M, Mancini Steven J, Clayworth Katherine V, Arbabi Keon, Beshara Simon
McMaster Integrative Neuroscience Discovery and Study (MiNDS) Program, McMaster University, Hamilton, ON, Canada.
Department of Psychology, Neuroscience & Behaviour, Faculty of Science, McMaster University, Hamilton, ON, Canada.
Front Cell Neurosci. 2020 Mar 17;14:56. doi: 10.3389/fncel.2020.00056. eCollection 2020.
An experience-driven increase in oligodendrocytes and myelin in the somatosensory cortex (S1) has emerged as a new marker of adult cortical plasticity. That finding contrasts with the view that myelin is a structural brake on plasticity, and that contributes to ending the critical period (CP) in the visual cortex (V1). Despite the evidence that myelin-derived signaling acts to end CP in V1, there is no information about myelin changes during adult plasticity in V1. To address this, we quantified the effect of three manipulations that drive adult plasticity (monocular deprivation (MD), fluoxetine treatment or the combination of MD and fluoxetine) on the expression of myelin basic protein (MBP) in adult rat V1. In tandem, we validated that environmental enrichment (EE) increased cortical myelin by measuring MBP in adult S1. For comparison with the MBP measurements, three plasticity markers were also quantified, the spine markers drebrin E and drebrin A, and a plasticity maintenance marker Ube3A. First, we confirmed that EE increased MBP in S1. Next, that expression of the plasticity markers was affected in S1 by EE and in V1 by the visual manipulations. Finally, we found that after adult MD, MBP increased in the non-deprived V1 hemisphere, but it decreased in the deprived hemisphere, and those changes were not influenced by fluoxetine. Together, the findings suggest that modulation of myelin expression in adult V1 may reflect the levels of visually driven activity rather than synaptic plasticity caused by adult plasticity.
体感皮层(S1)中少突胶质细胞和髓磷脂数量因经验驱动而增加,已成为成年皮层可塑性的一个新标志。这一发现与髓磷脂是可塑性的结构制动器这一观点形成对比,且髓磷脂有助于终止视觉皮层(V1)的关键期(CP)。尽管有证据表明髓磷脂衍生信号作用于终止V1的关键期,但关于V1成年可塑性过程中的髓磷脂变化尚无相关信息。为解决这一问题,我们量化了三种驱动成年可塑性的操作(单眼剥夺(MD)、氟西汀治疗或MD与氟西汀联合使用)对成年大鼠V1中髓磷脂碱性蛋白(MBP)表达的影响。同时,我们通过测量成年S1中的MBP来验证环境富集(EE)可增加皮层髓磷脂。为与MBP测量结果进行比较,还对三种可塑性标志物进行了量化,即棘突标志物 drebrin E和drebrin A,以及一种可塑性维持标志物Ube3A。首先,我们证实EE增加了S1中的MBP。其次,EE影响了S1中可塑性标志物的表达,而视觉操作影响了V1中可塑性标志物的表达。最后,我们发现成年MD后,未剥夺的V1半球中MBP增加,但剥夺半球中MBP减少,且这些变化不受氟西汀影响。总之,这些发现表明成年V1中髓磷脂表达的调节可能反映视觉驱动活动的水平,而非成年可塑性引起的突触可塑性。