TY - JOUR
T1 - Neuroprotective utility and neurotrophic action of neurturin in postnatal motor neurons
T2 - Comparison with GDNF and persephin
AU - Bilak, Masako M.
AU - Shifrin, David A.
AU - Corse, Andrea M.
AU - Bilak, Stephan R.
AU - Kuncl, Ralph W.
N1 - Funding Information:
We especially thank E. Johnson, J. Milbrandt, and P. Osborne (Washington University, St. Louis, MO) for providing neurturin and persephin and P. Kotzbauer for arranging the collaboration. M. Lehar provided technical help. This work was supported by research grants from the NINDS and the Muscular Dystrophy Association, an NINDS clinician investigator development award (to A.M.C.), the Cal Ripken/ Lou Gehrig Fund for Neuromuscular Research, and the Jay Slotkin Fund for Neuromuscular Research.
PY - 1999/5
Y1 - 1999/5
N2 - Neurturin and persephin are recently discovered homologs of glial cell line-derived neurotrophic factor (GDNF). Here, we report that neurturin, like GDNF, increases the choline acetyltransferase activity of normal postnatal motor neurons, induces neurite outgrowth in spinal cord, and potently protects motor neurons from chronic glutamate-mediated degeneration. Persephin, in contrast, does not appear to have neurotrophic or neurite- promoting effects on mature motor neurons and may instead worsen the glutamate injury of motor neurons. This pattern in the TGF-β family suggests certain receptor specificities, requiring at least the Ret/GFRα-1 receptor complex. The results predict potential benefit of neurturin, but not persephin, in the treatment of motor neuron disorders and spinal cord diseases.
AB - Neurturin and persephin are recently discovered homologs of glial cell line-derived neurotrophic factor (GDNF). Here, we report that neurturin, like GDNF, increases the choline acetyltransferase activity of normal postnatal motor neurons, induces neurite outgrowth in spinal cord, and potently protects motor neurons from chronic glutamate-mediated degeneration. Persephin, in contrast, does not appear to have neurotrophic or neurite- promoting effects on mature motor neurons and may instead worsen the glutamate injury of motor neurons. This pattern in the TGF-β family suggests certain receptor specificities, requiring at least the Ret/GFRα-1 receptor complex. The results predict potential benefit of neurturin, but not persephin, in the treatment of motor neuron disorders and spinal cord diseases.
UR - http://www.scopus.com/inward/record.url?scp=0032994474&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032994474&partnerID=8YFLogxK
U2 - 10.1006/mcne.1999.0756
DO - 10.1006/mcne.1999.0756
M3 - Article
C2 - 10356295
AN - SCOPUS:0032994474
SN - 1044-7431
VL - 13
SP - 326
EP - 336
JO - Molecular and Cellular Neurosciences
JF - Molecular and Cellular Neurosciences
IS - 5
ER -