I'm looking for information about callosal-corticospinal connections in mouse motor and sensory cortical areas and if there are any works about a possible modification, in terms of axons or synapses, after spinal cord lesion and subsequent exercise. I'm also not sure about the percentage of callosal motor and sensory fibers representation in mouse and at which extent their are connected with corticospinal neurons and what is the functional meaning of that.
hi,
a good place to start. http://onlinelibrary.wiley.com/doi/10.1111/nyas.12052/epdf
and http://www.rehab.research.va.gov/JOUR/08/45/2/pdf/Lynskey.pdf hope you find them useful.
and a review article by M. Oudega \nd M. Perez from Miami project where they elaborate the meaning of cortical reorganisation on functionalm outcomes. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3476625/
Hi Matilde,
allow me pls to revisit your question. I have to admit, your question resonated with me all the past time, it is so specific and on target, I think you are on to something brilliant, allegiant and plausible, but what kept bothering me is the paradigm of exercise training reported in the literature (wheel walking, bicycling, or step training on a treadmill) in order to display different qualities of neuronal plasticity, and locomotor recovery. The ability of over ground weight bearing stimulation to generate effective stepping is attributed frequently to the activation of neural circuits in the spinal cord responsible for central pattern generation, i.e., circuits that generate coordinated alternating flexor-extensor neuromotor patterns in the absence of supraspinal or sensory modulation. (Van de Crommert H.W. et al. 1998) Central pattern generation certainly has an important role in locomotion, but when the injury spares the locomotor circuitry and afferent inputs, sensory information, e.g., proprioceptive, cutaneous, etc., can be equally, if not more, important in shaping the recovered locomotor patterns. One Effective execution of weight-bearing stepping in spinal subjects appears to be accomplished when the spinal locomotor circuits are modulated by stepping-associated sensory input. The important point is that the stimulation parameters can be rather nonspecific if the sensory input associated with stepping is available to provide the fine tuning as processing of proprioceptive input provides a remarkable means of coordinating massive amounts of dynamic sensory information projecting to the motor pools that generate stepping. (Fong, A.J. et al. 2009)
Namely the forced swim exercise, where the animals are forced to swim without an escape, the fear of drowning generates a sufficient stress that induces a significant increase in 5-HT1A receptor mRNA levels in the brainstem, frontal motor cortex and hippocampus (Shishkina et al., 2012). In order for the hind limbs to follow through in the entire swim, an intact continuum of the corticospinal pathway must be established to carry the neural signals down to the animals’ hind limbs suffice to move the hind limbs against the resistance of water. Such details cannot be described by wheel walking, bicycling, or step training on a treadmill.
To the best of my knowledge, one single report on the effect of swim training following SCI on sensory function. (Hutchinson, K.J. et al 2004).
May I suggest: moderate spinal cord injury, swim training, and control untrained. Exercise training begins 6 days post-SCI, duration 6 + 6 min per day, 6 days a week for 6 weeks. Best wishes to you on your research. Hope I helped you with your question.
Good luck.
Ghanim.
http://www.ncbi.nlm.nih.gov/pubmed/23320512,19660669,20809785,23531013,15069022,25774179,10200392,22982152
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