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Almutairi, Alhumaid, Roach, Gates, and Fuller: What is the relationship between survival motor neuron expression and rat spinal cord development?

Introduction: Spinal Muscular Atrophy (SMA) is the leading genetic killer of young infants. It is characterized by degeneration of the lower motor neurons in the spinal cord and brain stem and is caused by a defect in the survival motor neuron (SMN) gene. Recently, research has shown that there is a relation between SMA and defects in sensory neurons.

Objective: To understand the temporal and spatial expression of the SMN protein during development of the rat spinal cord, in order to develop an understanding of the role of SMN protein in sensory and motor areas of the spinal cord.

Material and methods: Rat spinal cord cross sections from cervical, thoracic and lumbar levels were obtained from rats at postnatal (P) days P21, P14, P10, P7, P5, P3 and P0. Indirect immunohistochemistry was performed using a monoclonal antibody against SMN to observe its expression in the developing spinal cord.

Results: SMN expression in the dorsal funiculus increased during postnatal development, with a peak expression occurring at P14 and continuing into early adulthood. SMN staining of the corticospinal tract was noted at only early adulthood and was undetectable at the developmental time points investigated.

Conclusions: The pattern of SMN expression during development in the dorsal funiculus proper and corticospinal tract correlates with the known changes that occur in the number and myelination status of axons in these areas. The staining of sections showed that there is a high level of SMN expression at a time when the number of axons are known to decrease. This pattern of SMN expression suggests that it may be involved in fine-tuning of the sensory–motor circuitry, and may also be related to the maturation of sensory–motor axons. These findings support the notion that SMN is an important protein for the development of the sensory–motor pathway.

Acknowledgements: We would like to thank Dr Heidi R Fuller and Dr Monte A Gates for their guidance, support and help.

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