Clowry GJ

Galley S

A CST-YFP transgenic mouse has been developed for the study of the corticospinal tract in which yellow fluorescent protein is expressed under the control of thy1 and emx1 promoters in order to restrict expression to fore-brain neurones. We explored plasticity of the developing corticospinal tract of these mice following a unilateral lesion to the sensorimotor cortex at postnatal day 7. The extent of innervation of the cervical spinal cord at time points post-lesion was assessed by measuring density of immunoperoxidase reactivity for yellow fluorescent protein in the dorsal funiculi and a defined region of each dorsal horn, and by counting immunoreactive axonal varicosities in the ventral horns. Two/three days post-lesion, the density of immunoreactivity in the dorsal horn contralateral to the lesion was reduced proportional to the decrease in positive fibres in the dorsal funiculus, however density of immunoreactive varicosities in the ventral horn was more resistant to loss. Over a three week period, immunoreactive axonal processes in the grey matter increased on the contralateral side, particularly in the ventral horn, but without an increase in immunopositive fibres in the contralateral dorsal funiculus, demonstrating sprouting of surviving immunoreactive fibres to replace lesioned corticospinal axons. However, the origin of sprouting fibres could not be identified with confidence as parallel observations revealed strongly immunoreactive neuronal cell bodies in the spinal cord, medulla and red nucleus. We have demonstrated plasticity in response to a developmental lesion but discovered a drawback to using these mice if visualisation of individual axons is enhanced by immunohistochemistry

Plasticity to neonatal sensorimotor cortex injury: Plasticity to neonatal sensorimotor cortex injury in the YFP-CST mouse

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