Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice.
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Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice. / Sibbe, Mirjam; Taniguchi, M; Schachner, Melitta; Bartsch, Udo.
In: NEUROSCIENCE, Vol. 150, No. 4, 4, 2007, p. 898-904.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice.
AU - Sibbe, Mirjam
AU - Taniguchi, M
AU - Schachner, Melitta
AU - Bartsch, Udo
PY - 2007
Y1 - 2007
N2 - Mutations in the gene encoding the neural recognition molecule L1 result in hypoplasia of the corticospinal tract and path finding errors of corticospinal axons at the pyramidal decussation. Candidate molecules that have been implicated in L1-dependent guidance of corticospinal axons from the ventral medullary pyramids to the contralateral dorsal columns of the cervical spinal cord include Semaphorin3A and CD24. In the present study, we anterogradely labeled corticospinal axons from the sensorimotor cortex of young postnatal Semaphorin3A- and CD24-deficient mice to elucidate potential functions of both proteins during formation of this long axon projection. Our results indicate that elongation, collateralization, fasciculation and path finding of corticospinal axons in mice proceed normally in the absence of Semaphorin3A or CD24.
AB - Mutations in the gene encoding the neural recognition molecule L1 result in hypoplasia of the corticospinal tract and path finding errors of corticospinal axons at the pyramidal decussation. Candidate molecules that have been implicated in L1-dependent guidance of corticospinal axons from the ventral medullary pyramids to the contralateral dorsal columns of the cervical spinal cord include Semaphorin3A and CD24. In the present study, we anterogradely labeled corticospinal axons from the sensorimotor cortex of young postnatal Semaphorin3A- and CD24-deficient mice to elucidate potential functions of both proteins during formation of this long axon projection. Our results indicate that elongation, collateralization, fasciculation and path finding of corticospinal axons in mice proceed normally in the absence of Semaphorin3A or CD24.
M3 - SCORING: Zeitschriftenaufsatz
VL - 150
SP - 898
EP - 904
JO - NEUROSCIENCE
JF - NEUROSCIENCE
SN - 0306-4522
IS - 4
M1 - 4
ER -