Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 37, Issue 1, Pages 143-152Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2007.09.005
Keywords
plasminogen activator; crossed phrenic phenomenon; knockout mice; synaptic plasticity; diaphragmatic function
Categories
Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [T32NS007083] Funding Source: NIH RePORTER
- NINDS NIH HHS [NS441219, T32-NS007083] Funding Source: Medline
Ask authors/readers for more resources
The possibility that plasminogen activator (PA) plays a role in synaptic plasticity was explored in the spinal cord during the crossed phrenic phenomenon (CPP), where respiratory functional plasticity develops following spinal cord injury. Synaptic remodeling on phrenic motor-neurons occurs during the characteristic delay period following spinal cord injury before CPP recovery of respiratory function. The molecular mechanisms underlying this plasticity are not well-defined. During the critical 1-2 h delay period required for this synaptic plasticity following a C2 hemisection in mice, uPA and tPA mRNAs are rapidly induced in C4-5 ventral spinal cord neurons in the ipsilateral phrenic motor nucleus (PMN), as are uPA and tPA protein levels. A role for uPA in CPP spinal cord plasticity is confirmed by the impaired ability of uPA knockout mice to acquire a good CPP response by 6 h post-hemisection and their lack of structural remodeling of PMN synapses that underlies development of the CPP response. (C) 2007 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available