PMID- 19437548
OWN - NLM
STAT- MEDLINE
DCOM- 20100112
LR  - 20090818
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 87
IP  - 13
DP  - 2009 Oct
TI  - Mitochondrial cytochrome c oxidase expression in the central nervous system is 
      elevated at sites of pressure gradient elevation but not absolute pressure 
      increase.
PG  - 2973-82
LID - 10.1002/jnr.22120 [doi]
AB  - The paucity of suitable experimental models has made it difficult to isolate the 
      pathogenic role of mitochondria in central nervous system diseases associated 
      with absolute pressure elevation and increased pressure gradients. Experimental 
      models of traumatic brain injury (TBI) and hydrocephalus have been useful for 
      examining the mitochondrial response following pressure increase in the central 
      nervous system; however, the presence of multiple pathogenic factors acting on 
      the brain in these previous studies has made it difficult to determine whether 
      the induced changes were a result of mechanical damage, intracranial pressure 
      elevation, or other pathogenic factors. By direct monitoring and control of 
      pressures in the intraocular, intracranial, and vascular compartments, we use the 
      pig optic nerve, a typical central white matter tract, to compare the temporal 
      sequence of cytochrome c oxidase (CcO) levels between regions of absolute 
      pressure elevation and pressure gradient increase. We demonstrate that a rise in 
      pressure gradient without traumatic injury up-regulates CcO levels across the 
      site of the gradient, in a manner similar to what has been previously reported 
      for hydrocephalus. We also demonstrate that CcO changes do not occur following an 
      absolute pressure rise. These findings taken together with our recent reports 
      suggest that mitochondria initiate an early compensatory response to axonal 
      damage following pressure gradient increase. Extrapolation of our results also 
      suggests that decreased CcO levels in TBI may be secondary to mechanical damage. 
      This study emphasises the importance of pressure gradients in regulating 
      mitochondrial function in the central nervous system.
CI  - 2009 Wiley-Liss, Inc.
FAU - Balaratnasingam, Chandrakumar
AU  - Balaratnasingam C
AD  - Centre for Ophthalmology and Visual Science and the ARC Centre of Excellence in 
      Vision Science, The University of Western Australia, Perth, Western Australia, 
      Australia.
FAU - Pham, Duy
AU  - Pham D
FAU - Morgan, William H
AU  - Morgan WH
FAU - Bass, Louise
AU  - Bass L
FAU - Cringle, Stephen J
AU  - Cringle SJ
FAU - Yu, Dao-Yi
AU  - Yu DY
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Nerve Tissue Proteins)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
SB  - IM
MH  - Animals
MH  - Axonal Transport
MH  - Blood Pressure
MH  - Cytoskeleton/metabolism/ultrastructure
MH  - Electron Transport Complex IV/*biosynthesis/genetics
MH  - Female
MH  - Gene Expression Regulation/*physiology
MH  - *Intracranial Pressure
MH  - *Intraocular Pressure
MH  - Mitochondria/*enzymology
MH  - Nerve Tissue Proteins/*biosynthesis/genetics
MH  - Ocular Hypertension/*enzymology/pathology
MH  - Optic Nerve/*enzymology/ultrastructure
MH  - Reproducibility of Results
MH  - Sus scrofa
EDAT- 2009/05/14 09:00
MHDA- 2010/01/13 06:00
CRDT- 2009/05/14 09:00
PHST- 2009/05/14 09:00 [entrez]
PHST- 2009/05/14 09:00 [pubmed]
PHST- 2010/01/13 06:00 [medline]
AID - 10.1002/jnr.22120 [doi]
PST - ppublish
SO  - J Neurosci Res. 2009 Oct;87(13):2973-82. doi: 10.1002/jnr.22120.