Rat motor neurons caudal to a rubrospinal tract (RST) transection remain viable

• Published in: Neuroscience Vol. 364; pp. 157 - 163
• Main Authors: Wild, Brandon M., Mohan, Rahul, Morris, Renée
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 19.11.2017
• Subjects: Animals; cervical; Cervical Cord - physiology; Efferent Pathways - injuries; Female; lumbar; Lumbar Vertebrae; motor neurons; Motor Neurons - physiology; rat; Rats; Rats, Long-Evans; Red Nucleus - physiology; rubrospinal tract; Spinal Cord - physiology; Spinal Cord Ventral Horn - physiology; stereology; motor neurons; lumbar; CE; RST; rat; ANOVA; rubrospinal tract; SCI; stereology; cervical; RN; DLF
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2017.09.013

•Spinal cord motor neurons do not undergo cell death up to 14days following a loss in supraspinal input.•There are no differences in population in both ipsilateral and contralateral ventral horns after a unilateral transection.•Motor neuron populations in both spinal cord segments C5-6 and L2-3 showed no significant changes following injury. In the rat, the rubrospinal tract (RST) is a descending motor pathway involved in the production of skilled reaching movement. The RST originates in the red nucleus in the midbrain and runs down the spinal cord in the lateral most aspect of the dorsolateral funiculus (DLF). The RST makes monosynaptic contact with interneurons within the intermediate laminae of the cord, however a contingent of RST axons constitutes direct supraspinal input for spinal cord motor neurons. The current study investigated the effects of unilateral RST transection at cervical levels C3-4 on the population of motor neurons in both spinal segments C5-6 and L2-3. The total number of large, medium and small motor neurons in these segments was estimated with stereological techniques in both ventral horns at 1, 3, 7 and 14days post-injury. In both spinal cord segments under investigation, no change was detected in mean number of motor neurons over time, in either ventral horn. That the loss of direct supraspinal input resulting from the RST transection does not affect the viability of motor neurons caudal to the injury indicates that these neurons have the potential to be re-innervated, should the RST injury be repaired.