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Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation.

Publication ,  Journal Article
Leslie, JR; Imai, F; Fukuhara, K; Takegahara, N; Rizvi, TA; Friedel, RH; Wang, F; Kumanogoh, A; Yoshida, Y
Published in: Development
September 2011

Different types of sensory neurons in the dorsal root ganglia project axons to the spinal cord to convey peripheral information to the central nervous system. Whereas most proprioceptive axons enter the spinal cord medially, cutaneous axons typically do so laterally. Because heavily myelinated proprioceptive axons project to the ventral spinal cord, proprioceptive axons and their associated oligodendrocytes avoid the superficial dorsal horn. However, it remains unclear whether their exclusion from the superficial dorsal horn is an important aspect of neural circuitry. Here we show that a mouse null mutation of Sema6d results in ectopic placement of the shafts of proprioceptive axons and their associated oligodendrocytes in the superficial dorsal horn, disrupting its synaptic organization. Anatomical and electrophysiological analyses show that proper axon positioning does not seem to be required for sensory afferent connectivity with motor neurons. Furthermore, ablation of oligodendrocytes from Sema6d mutants reveals that ectopic oligodendrocytes, but not proprioceptive axons, inhibit synapse formation in Sema6d mutants. Our findings provide new insights into the relationship between oligodendrocytes and synapse formation in vivo, which might be an important element in controlling the development of neural wiring in the central nervous system.

Duke Scholars

Published In

Development

DOI

EISSN

1477-9129

Publication Date

September 2011

Volume

138

Issue

18

Start / End Page

4085 / 4095

Location

England

Related Subject Headings

  • Synaptic Transmission
  • Synapses
  • Spinal Cord Diseases
  • Spinal Cord
  • Signal Transduction
  • Sensory Receptor Cells
  • Semaphorins
  • Proprioception
  • Oligodendroglia
  • Neurogenesis
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Leslie, J. R., Imai, F., Fukuhara, K., Takegahara, N., Rizvi, T. A., Friedel, R. H., … Yoshida, Y. (2011). Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation. Development, 138(18), 4085–4095. https://doi.org/10.1242/dev.066076
Leslie, Jennifer R., Fumiyasu Imai, Kaori Fukuhara, Noriko Takegahara, Tilat A. Rizvi, Roland H. Friedel, Fan Wang, Atsushi Kumanogoh, and Yutaka Yoshida. “Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation.Development 138, no. 18 (September 2011): 4085–95. https://doi.org/10.1242/dev.066076.
Leslie JR, Imai F, Fukuhara K, Takegahara N, Rizvi TA, Friedel RH, et al. Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation. Development. 2011 Sep;138(18):4085–95.
Leslie, Jennifer R., et al. “Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation.Development, vol. 138, no. 18, Sept. 2011, pp. 4085–95. Pubmed, doi:10.1242/dev.066076.
Leslie JR, Imai F, Fukuhara K, Takegahara N, Rizvi TA, Friedel RH, Wang F, Kumanogoh A, Yoshida Y. Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation. Development. 2011 Sep;138(18):4085–4095.
Journal cover image

Published In

Development

DOI

EISSN

1477-9129

Publication Date

September 2011

Volume

138

Issue

18

Start / End Page

4085 / 4095

Location

England

Related Subject Headings

  • Synaptic Transmission
  • Synapses
  • Spinal Cord Diseases
  • Spinal Cord
  • Signal Transduction
  • Sensory Receptor Cells
  • Semaphorins
  • Proprioception
  • Oligodendroglia
  • Neurogenesis