| Overstimulation by excess glutamate acting on its receptors is a causative agent in the secondary loss of tissue after weight-drop trauma to the spinal cord (SCI) in the adult rat. Additionally, protein levels of specific glutamate receptor subunits have been shown to be altered as a result of such injury. Glutamate receptor subunit mRNA is more highly expressed in the rat spinal cord during the first 2–3 weeks after birth. My hypothesis was that protein expression of these subunits was also elevated during this same period. Using quantitative western blot analysis, I found that subunit protein expression in the spinal cord was indeed higher during this period compared to adult. This led me to the hypothesis that the effects of the excess glutamate released after SCI would be exacerbated in young rats compared to adult. I characterized a model of weight-drop SCI in Sprague-Dawley rats at postnatal day 14–15 (P14–15), which was found to produce an initial contusion that was quite similar to that seen previously in adults. The injury I produced, like that in adults was reproducible and graded, in that impact from increasing height produced greater functional deficit. I found the functional deficit after SCI using a 10 g weight dropped from a height of 2.5 cm leads to functional deficits in young rats that were similar to those previously observed in adults. I also discovered that there was delayed loss of ventral motor neurons and rapid recovery of hindlimb function (as measured by locomotor and sensorimotor function) compared to adult animals subjected to a similar injury. Additionally, there was a decrease in glutamate receptor subunit protein that showed a different pattern and time course than that seen in adult rats after similar injury. In summary, glutamate receptor subunit expression, tissue loss after SCI, functional plasticity after SCI, and the responsive decrease in glutamate receptor subunits after SCI are all altered in 2 week old pups as compared to adult rats. |
