Xu X M, Martin G F
Department of Anatomy, Ohio State University, College of Medicine, Columbus 43210.
J Comp Neurol. 1989 Jan 15;279(3):368-81. doi: 10.1002/cne.902790304.
We have shown previously that rubral axons can grow caudal to a lesion of their pathway at thoracic levels of the spinal cord in the developing opossum, Didelphis virginiana. In the present report we expand on that observation and present evidence which suggests that the critical period for plasticity of the rubrospinal tract ends earlier at cervical than at thoracic levels. In addition, we show that most rubrospinal neurons die as a result of axotomy during early stages of the critical period. The opossum was chosen for study because the development of its rubrospinal tract occurs after birth. In one set of experiments the area containing the rubrospinal tract was lesioned at cervical or thoracic levels and after 30 days or more, retrograde transport techniques were used to determine if rubral axons had grown caudal to the lesion. When the lesions were made at rostral cervical levels between estimated postnatal day 26 and maturity, neurons could not be labeled in the contralateral red nucleus by injections of retrograde markers ipsilateral to the lesion and caudal to it. We were not able to obtain adequate survival after cervical lesions made prior to estimated postnatal day 26. When the lesions were made at mid to caudal thoracic levels between estimated postnatal days 19 and 26, neurons could be labeled in the contralateral red nucleus. When comparable lesions were made at estimated postnatal day 40, there was usually a decrease in the number of labeled neurons, and when they were made at estimated postnatal day 54, none was labeled. In selected cases, operated at estimated postnatal day 19, cell counts provided evidence for loss of neurons in the red nucleus contralateral to the lesion. In orthograde transport experiments performed on animals with thoracic lesions of the rubrospinal tract made between estimated postnatal days 18 and 33, rubral axons could be labeled caudal to the lesion, and they seemed to take the most direct route around it. Although they sometimes assumed abnormal positions caudal to the lesion, rubral axons appeared to reach areas of the gray matter appropriate to them. When lesions were made at estimated postnatal day 54 or in older animals, labeled axons could be traced to the lesion site but not caudal to it.(ABSTRACT TRUNCATED AT 400 WORDS)
我们之前已经表明，在发育中的弗吉尼亚负鼠脊髓胸段，红核轴突能够向其通路损伤部位的尾侧生长。在本报告中，我们扩展了这一观察结果，并提供证据表明，红核脊髓束可塑性的关键期在颈部比在胸段结束得更早。此外，我们表明，大多数红核脊髓神经元在关键期早期因轴突切断而死亡。选择负鼠进行研究是因为其红核脊髓束在出生后发育。在一组实验中，在颈部或胸段对包含红核脊髓束的区域进行损伤，30天或更长时间后，使用逆行运输技术来确定红核轴突是否向损伤部位的尾侧生长。当在估计出生后第26天至成熟之间的颈前部水平进行损伤时，通过在损伤同侧及其尾侧注射逆行标记物，无法在对侧红核中标记神经元。在估计出生后第26天之前进行颈部损伤后，我们无法获得足够的存活时间。当在估计出生后第19天至26天之间的胸段中后部水平进行损伤时，可以在对侧红核中标记神经元。当在估计出生后第40天进行类似损伤时，标记神经元的数量通常会减少，而在估计出生后第54天进行损伤时，则没有神经元被标记。在选定的病例中，于估计出生后第19天进行手术，细胞计数提供了损伤对侧红核中神经元丢失的证据。在对估计出生后第18天至33天之间进行红核脊髓束胸段损伤的动物进行的顺行运输实验中，红核轴突可以在损伤部位的尾侧被标记，并且它们似乎绕过损伤部位走最直接的路线。尽管它们有时在损伤部位的尾侧处于异常位置，但红核轴突似乎到达了适合它们的灰质区域。当在估计出生后第54天或在年龄较大的动物中进行损伤时，标记的轴突可以追踪到损伤部位，但不能追踪到其尾侧。（摘要截断于400字）
