Normal development and post-traumatic plasticity of corticospinal neurons in rats

Abstract

Corticospinal (CS) neurons projecting to the spinal cord in the adult rat, identified by retrograde axonal transport of horseradish peroxidase (HRP), formed a caudal band in areas 3, 4, and 6 and a rostral band in area 10, separated by a gap. In the infant the gap was filled with CS neurons. The problem: What happened to the transient infant neurons as the mantle expanded, and would they persist if other CS neurons were destroyed in infancy? Identification of CS neurons by HRP and measurements of the growth of the mantle and cortical areas 3, 4, and 6 showed that CS neurons were scattered widely in the cortex as well as in the gap and future bands at 2 to 10 days. By about 2 weeks, CS neurons labeled from the cervical cord were limited to the "adult" bands. The greatest mantle expansion postnatally was in the occipital and bregma regions, including the anterior, but not the posterior, part of area 3, 4, and 6. Thus, expansion of the mantle, growth of areas 3, 4, and 6, and axonal growth of transient and permanent CS neurons did not parallel each other closely. When one or both caudal band regions were ablated at 5, 7, or 10 days, the gap CS neurons persisted bilaterally to adult life. No necrosis of layer V neurons was observed between 10 days and 2 weeks. It was assumed that the gap neurons and other extraneous CS neurons generated exploratory axons which normally disappeared, but when caudal band neurons were destroyed the transient axons attempted to fill the pathway.