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-
1 (TGF-
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-
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
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