 |
|||||
|
|||||
|
|||||
|
|||||
|
|||||
The Journal of Neuroscience, April 19, 2006, 26(16):4406-4414; doi:10.1523/JNEUROSCI.5467-05.2006
Previous Article | Next Article
Development/Plasticity/Repair
Chondroitinase ABC Digestion of the Perineuronal Net Promotes Functional Collateral Sprouting in the Cuneate Nucleus after Cervical Spinal Cord Injury
James M. Massey,1,2,3,4 Charles H. Hubscher,2,4 Michelle R. Wagoner,3,4 Julie A. Decker,3,4 Jeremy Amps,5 Jerry Silver,5 andStephen M. Onifer2,3,4 1MD/PhD Program, Departments of2 Anatomical Sciences and Neurobiology and 3Neurological Surgery, and 4Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, Kentucky 40292, and 5Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
Correspondence should be addressed to Dr. Stephen M. Onifer, Spinal Cord and Brain Injury Research Center, University of Kentucky, Biomedical and Biological Sciences Research Building B365, 741 South Limestone Street, Lexington, KY 40536-0509. Email: stephen.onifer{at}uky.edu
Upregulation of extracellular chondroitin sulfate proteoglycans (CSPGs) after CNS injuries contributes to the impediment of functional recovery by restricting both axonal regeneration and synaptic plasticity. In the present study, the effect of degrading CSPGs with the application of the bacterial enzyme chondroitinase ABC (chABC) into the cuneate nucleus of rats partially denervated of forepaw dorsal column axons was examined. A dorsal column transection between the C6–C7 dorsal root entry zones was followed immediately by an ipsilateral brainstem injection of either chABC or a bacterial-derived control enzyme [penicillinase (P-ase)] and then subsequently (1 week later) followed with a second brainstem enzyme injection and cholera toxin B subunit (CTB) tracer injection into the ipsilateral forepaw digits and pads. After 1 additional week, the rats underwent electrophysiological receptive field mapping of the cuneate nucleus and/or anatomical evaluation. Examination of the brainstems of rats from each group revealed that CSPGs had been reduced after chABC treatment. Importantly, in the chABC-treated rats (but not in the P-ase controls), a significantly greater area of the cuneate nucleus was occupied by physiologically active CTB traced forepaw afferents that had been spared by the initial cord lesion. These results demonstrate, for the first time, a functional change directly linked to anatomical evidence of sprouting by spinal cord afferents after chABC treatment.
Key words: somatosensory system; proteoglycan; axonal regeneration; synaptic plasticity; synaptogenesis; extracellular matrix; receptive field; microelectrode; dorsal columns
Received Dec. 21, 2005; revised Feb. 21, 2006; accepted March 19, 2006.
Correspondence should be addressed to Dr. Stephen M. Onifer, Spinal Cord and Brain Injury Research Center, University of Kentucky, Biomedical and Biological Sciences Research Building B365, 741 South Limestone Street, Lexington, KY 40536-0509. Email: stephen.onifer{at}uky.edu
This article has been cited by other articles:
Y. Shen, A. P. Tenney, S. A. Busch, K. P. Horn, F. X. Cuascut, K. Liu, Z. He, J. Silver, and J. G. Flanagan
PTP{sigma} Is a Receptor for Chondroitin Sulfate Proteoglycan, an Inhibitor of Neural Regeneration
Science, October 23, 2009; 326(5952): 592 - 596.
[Abstract] [Full Text] [PDF]
S. A. Busch, K. P. Horn, D. J. Silver, and J. Silver
Overcoming Macrophage-Mediated Axonal Dieback Following CNS Injury
J. Neurosci., August 12, 2009; 29(32): 9967 - 9976.
[Abstract] [Full Text] [PDF]
W. R. Reed, H. K. Chadha, and C. H. Hubscher
Effects of 17{beta}-Estradiol on Responses of Viscerosomatic Convergent Thalamic Neurons in the Ovariectomized Female Rat
J Neurophysiol, August 1, 2009; 102(2): 1062 - 1074.
[Abstract] [Full Text] [PDF]
L. M. Carter, M. L. Starkey, S. F. Akrimi, M. Davies, S. B. McMahon, and E. J. Bradbury
The Yellow Fluorescent Protein (YFP-H) Mouse Reveals Neuroprotection as a Novel Mechanism Underlying Chondroitinase ABC-Mediated Repair after Spinal Cord Injury
J. Neurosci., December 24, 2008; 28(52): 14107 - 14120.
[Abstract] [Full Text] [PDF]
W. B. J. Cafferty, E. J. Bradbury, M. Lidierth, M. Jones, P. J. Duffy, S. Pezet, and S. B. McMahon
Chondroitinase ABC-Mediated Plasticity of Spinal Sensory Function
J. Neurosci., November 12, 2008; 28(46): 11998 - 12009.
[Abstract] [Full Text] [PDF]
K. J. Cothron, J. M. Massey, S. M. Onifer, and C. H. Hubscher
Identification of penile inputs to the rat gracile nucleus
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2008; 294(3): R1015 - R1023.
[Abstract] [Full Text] [PDF]
M. Brus-Ramer, J. B. Carmel, S. Chakrabarty, and J. H. Martin
Electrical Stimulation of Spared Corticospinal Axons Augments Connections with Ipsilateral Spinal Motor Circuits after Injury
J. Neurosci., December 12, 2007; 27(50): 13793 - 13801.
[Abstract] [Full Text] [PDF]
J. FitzGerald and J. Fawcett
Repair in the central nervous system
J Bone Joint Surg Br, November 1, 2007; 89-B(11): 1413 - 1420.
[Abstract] [Full Text] [PDF]
C. M. Galtrey, R. A. Asher, F. Nothias, and J. W. Fawcett
Promoting plasticity in the spinal cord with chondroitinase improves functional recovery after peripheral nerve repair
Brain, April 1, 2007; 130(4): 926 - 939.
[Abstract] [Full Text] [PDF]
A. W. Barritt, M. Davies, F. Marchand, R. Hartley, J. Grist, P. Yip, S. B. McMahon, and E. J. Bradbury
Chondroitinase ABC Promotes Sprouting of Intact and Injured Spinal Systems after Spinal Cord Injury.
J. Neurosci., October 18, 2006; 26(42): 10856 - 10867.
[Abstract] [Full Text] [PDF]
J. D. Houle, V. J. Tom, D. Mayes, G. Wagoner, N. Phillips, and J. Silver
Combining an autologous peripheral nervous system "bridge" and matrix modification by chondroitinase allows robust, functional regeneration beyond a hemisection lesion of the adult rat spinal cord.
J. Neurosci., July 12, 2006; 26(28): 7405 - 7415.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|