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Ichikawa, H. et al.

H. Ichikawa, R. Terayama, T. Yamaai, Y. De Repentigny, R. Kothary, T. Sugimoto,

The number of nociceptors in the trigeminal ganglion but not proprioceptors in the mesencephalic trigeminal tract nucleus is reduced in dystonin deficient dystonia musculorum mice.

The trigeminal ganglion (TG) and mesencephalic trigeminal tract nucleus (Mes5) were investigated in wild type and dystonia musculorum (dt) mice to study the effect of dystonin deficiency on primary sensory neurons in the trigeminal nervous system. At postnatal day 14, the number of TG neurons was markedly decreased in dt mice when compared to wild type mice (43.1% reduction). In addition, dystonin disruption decreased the number of sensory neurons which bound to isolectin B4, and contained calcitonin gene-related peptide or high-affinity nerve growth factor receptor TrkA. Immunohistochemistry for caspase-3 demonstrated that dystonin deficiency induced excess cell death of TG neurons during the early postnatal period. In contrast, Mes5 neurons were barely affected in dt mice. These data together suggest that dystonin is necessary for survival of nociceptors but not proprioceptors in the trigeminal nervous system.[1]

References

The number of nociceptors in the trigeminal ganglion but not proprioceptors in the mesencephalic trigeminal tract nucleus is reduced in dystonin deficient dystonia musculorum mice. Ichikawa, H., Terayama, R., Yamaai, T., De Repentigny, Y., Kothary, R., Sugimoto, T. Brain Res. (2008) [Pubmed]

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