Kim Soo Young, Jones Theresa A
Institute for Neuroscience, University of Texas at Austin, Austin, Texas 78712, USA.
Synapse. 2010 Sep;64(9):659-71. doi: 10.1002/syn.20777.
In young adult rats, unilateral lesions of the sensorimotor cortex lead to neuronal structural plasticity and synaptogenesis in the contralateral motor cortex, which is connected to the lesion site by transcallosal fibers. The contralesional neural plasticity varies with lesion size and results from the convergence of denervation-induced reactive plasticity and behavioral asymmetries. It was unknown whether similar effects occur in older animals. Furthermore, the coordination of synaptic responses with that of perisynaptic astrocytes had not been investigated. In this study, middle-aged rats (14-16 months old) were given sham-operations or unilateral ischemic lesions of the sensorimotor cortex. Fifty days later, numerical densities of neurons and synapses and morphological characteristics of astrocytic processes in layer V of the contralesional motor cortex were measured using stereological light and electron microscopy methods. Lesions resulted in behavioral asymmetries, but no significant synapse addition in the contralesional motor cortex. Synapse number per neuron was negatively correlated with lesion size and reduced opposite larger lesions compared with smaller ones. Astrocytic changes were also lesion size-dependent. Astrocytic hypertrophy was observed only after smaller lesions and was associated with greater coverage and greater numbers of synapses. These findings are consistent with those in younger rats indicating an inverse relationship between lesion size and adaptive neuronal restructuring in denervated cortex. However, they indicate that the synaptogenic reaction to this lesion is relatively limited in older animals. Finally, the results indicate that structural plasticity of perisynaptic astrocytes parallels, and could play a role in shaping, synaptic responses to postischemic denervation.
在年轻成年大鼠中，感觉运动皮层的单侧损伤会导致对侧运动皮层发生神经元结构可塑性和突触形成，对侧运动皮层通过胼胝体纤维与损伤部位相连。对侧神经可塑性随损伤大小而变化，是去神经支配诱导的反应性可塑性和行为不对称性共同作用的结果。尚不清楚在老年动物中是否会出现类似的效应。此外，突触反应与突触周围星形胶质细胞的反应之间的协调性尚未得到研究。在本研究中，对中年大鼠（14 - 16个月大）进行假手术或感觉运动皮层的单侧缺血性损伤。50天后，使用体视学光镜和电镜方法测量对侧运动皮层V层神经元和突触的数值密度以及星形胶质细胞突起的形态特征。损伤导致行为不对称，但对侧运动皮层中没有明显的突触增加。每个神经元的突触数量与损伤大小呈负相关，与较小损伤相比，较大损伤对侧的突触数量减少。星形胶质细胞的变化也取决于损伤大小。仅在较小损伤后观察到星形胶质细胞肥大，且与更大的覆盖范围和更多的突触数量相关。这些发现与年轻大鼠中的发现一致，表明去神经支配皮层中损伤大小与适应性神经元重构之间存在反比关系。然而，这些发现表明老年动物对这种损伤的突触形成反应相对有限。最后，结果表明突触周围星形胶质细胞的结构可塑性与缺血后去神经支配的突触反应平行，并且可能在塑造突触反应中发挥作用。
