PMID- 18001202
OWN - NLM
STAT- MEDLINE
DCOM- 20080227
LR  - 20091119
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 24
IP  - 11
DP  - 2007 Nov
TI  - Prolonged microgliosis in the rhesus monkey central nervous system after 
      traumatic brain injury.
PG  - 1719-42
AB  - Impaired fine motor functions after traumatic brain injury (TBI) in humans and 
      non-human primates often continue to improve months after injury. To initiate a 
      series of studies in the primate model designed to investigate possible 
      involvement of microglia/macrophage in the long-term recovery processes, changes 
      in these cells were studied in the rhesus monkey central nervous system at 1, 6, 
      and 12 months after a combined unilateral lesion of the arm area of the primary 
      motor cortex and arm area of the lateral premotor cortex. Immunohistological 
      studies showed profound CD68 immunoreactivity in the lesion area and the 
      contralateral lateral corticospinal tract in the spinal cord at all time points, 
      demonstrating that microglia/macrophage remain reactive at the sites of injury 
      and axonal degeneration/survival for at least 12 months. We also observed marked 
      increases in brain-derived neurotrophic factor (BDNF) and its receptor subtypes, 
      TrkB[gp145] and TrkB[TK-], around the cortical lesion site after 6-month 
      survival. Similar increases were also observed in the spinal cord, although it 
      was less apparent for TrkB[gp145]. Double-labeling revealed that a subpopulation 
      of CD68-immunoreacitve microglia/macrophage co-expressed BDNF in the cortex and 
      spinal cord, and also TrkB[gp145] or TrkB[TK-] in the spinal cord. In contrast, 
      cytokine expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta 
      (IL-1beta), and interleukin-6 (IL-6) at these time intervals was less prominent, 
      suggesting that immediate inflammatory responses had subsided. These results 
      demonstrate that microglia/macrophage undergo prolonged activation after TBI in 
      the non-human primate brain and express BDNF and its receptors, suggesting their 
      tropic/trophic roles in the long-term recovery processes.
FAU - Nagamoto-Combs, Kumi
AU  - Nagamoto-Combs K
AD  - Department of Pharmacology, Physiology and Therapeutics, University of North 
      Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota 58202, 
      USA.
FAU - McNeal, David W
AU  - McNeal DW
FAU - Morecraft, Robert J
AU  - Morecraft RJ
FAU - Combs, Colin K
AU  - Combs CK
LA  - eng
GR  - NS 046367/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (CD68 antigen, human)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
EIN - J Neurotrauma. 2007 Dec;24(12):1889
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - Antigens, Differentiation, Myelomonocytic/metabolism
MH  - Brain Injuries/complications/metabolism/*pathology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cervical Vertebrae
MH  - Gliosis/*etiology/metabolism/pathology
MH  - Macaca mulatta
MH  - Macrophages/pathology
MH  - Male
MH  - Microglia/pathology
MH  - Receptor, trkB/metabolism
MH  - Spinal Cord/metabolism/*pathology
MH  - Time Factors
EDAT- 2007/11/16 09:00
MHDA- 2008/02/28 09:00
CRDT- 2007/11/16 09:00
PHST- 2007/11/16 09:00 [pubmed]
PHST- 2008/02/28 09:00 [medline]
PHST- 2007/11/16 09:00 [entrez]
AID - 10.1089/neu.2007.0377 [doi]
PST - ppublish
SO  - J Neurotrauma. 2007 Nov;24(11):1719-42. doi: 10.1089/neu.2007.0377.