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The Journal of Neuroscience, 0000, 20:RC77:1-5

RAPID COMMUNICATION
Cervical Dorsal Rhizotomy Increases Brain-Derived Neurotrophic Factor and Neurotrophin-3 Expression in the Ventral Spinal Cord

Rebecca A. Johnson1, Angela J. Okragly2, Mary Haak-Frendscho2, and Gordon S. Mitchell1

1 Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53706, and 2 Department of Neurobiology and Immunology, Promega Corporation, Madison, Wisconsin 53711

Although neurotrophic factors have been implicated in several forms of neuroplasticity, little is known concerning their potential role in spinal plasticity. Cervical dorsal rhizotomy (CDR) enhances serotonin terminal density near (spinal) phrenic motoneurons and serotonin-dependent long-term facilitation of phrenic motor output (Kinkead et al., 1998). We tested the hypothesis that selected neurotrophic factors change in a manner consistent with an involvement in this model of spinal plasticity. Brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), glial cell line-derived neurotrophic factor (GDNF), and transforming growth factor-beta 1 (TGF-beta 1) concentrations were measured (ELISA) in three regions of interest to respiratory control: (1) ventral cervical spinal segments associated with the phrenic motor nucleus (C3-C6), (2) ventral thoracic spinal segments associated with inspiratory intercostal motor output (T3-T6) and (3) the diaphragm. Tissues were harvested from rats 7 d after bilateral CDR and compared with sham-operated and unoperated control rats. CDR increased BDNF (110%; p = 0.002) and NT-3 (100%; p = 0.002) in the cervical and NT-3 in the thoracic spinal cord (98%; p = 0.009). GDNF and TGF-beta 1 were not altered by CDR in any tissue. Immunohistochemistry localized BDNF and NT-3 to motoneurons and interneurons of the ventral spinal cord. These studies provide novel, suggestive evidence that BDNF and NT-3, possibly through their trophic effects on serotonergic neurons and/or motoneurons, may underlie serotonin-dependent plasticity in (spinal) respiratory motor control after CDR.

Key words: plasticity; spinal; serotonin; respiratory control; phrenic motor nucleus; neurotrophin


Copyright © 0000 Society for Neuroscience  0270-6474/00/$05.00/0


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