PMID- 12359171
OWN - NLM
STAT- MEDLINE
DCOM- 20021017
LR  - 20211025
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 176
IP  - 2
DP  - 2002 Aug
TI  - Long-term locomotor training up-regulates TrkB(FL) receptor-like proteins, 
      brain-derived neurotrophic factor, and neurotrophin 4 with different topographies 
      of expression in oligodendroglia and neurons in the spinal cord.
PG  - 289-307
AB  - Neurotrophins are potent regulators of neuronal survival, maintenance, and 
      synaptic strength. In particular, brain-derived neurotrophic factor (BDNF), 
      acting through full-length TrkB receptor (TrkB(FL)), is implicated in the 
      stimulation of neurotransmission. Physical activity has been reported to increase 
      BDNF expression in the brain and spinal cord. In this study we have evaluated the 
      hypothesis that activation of a spinal neuronal network, due to exercise, affects 
      the entire spinal neurotrophin system acting via TrkB receptors by modulation of 
      BDNF, neurotrophin 4 (NT-4), and their TrkB receptor proteins. We investigated 
      the effect of treadmill walking (4 weeks, 1 km daily) on distribution patterns 
      and response intensity of these proteins in the lumbar spinal cord of adult rats. 
      Training enhanced immunoreactivity (IR) of both neurotrophins. BDNF IR increased 
      in cell processes of spinal gray matter, mainly in dendrites. NT-4 IR was 
      augmented in the white matter fibers, which were, in part, of astrocytic 
      identity. Training strongly increased both staining intensity and number of 
      TrkB(FL)-like IR small cells of the spinal gray matter. The majority of these 
      small cells were oligodendrocytes, representing both their precursor and their 
      mature forms. In contrast, training did not exert an effect on expression of the 
      truncated form of TrkB receptor in the spinal cord. These results show that both 
      neuronal and nonneuronal cells may be actively recruited to BDNF/NT-4/TrkB(FL) 
      neurotrophin signaling which can be up-regulated by training. Oligodendrocytes of 
      the spinal gray matter were particularly responsive to exercise, pointing to 
      their involvement in activity-driven cross talk between neurons and glia.
FAU - Skup, Malgorzata
AU  - Skup M
AD  - Department of Neurophysiology, Nencki Institute of Experimental Biology, Polish 
      Academy of Sciences, 3 Pasteur St. 02-093 Warsaw, Poland. mskup@nencki.gov.pl
FAU - Dwornik, Anna
AU  - Dwornik A
FAU - Macias, Matylda
AU  - Macias M
FAU - Sulejczak, Dorota
AU  - Sulejczak D
FAU - Wiater, Maciej
AU  - Wiater M
FAU - Czarkowska-Bauch, Julita
AU  - Czarkowska-Bauch J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cell Count
MH  - Immunohistochemistry
MH  - Lumbosacral Region
MH  - Male
MH  - Motor Activity/*physiology
MH  - Nerve Fibers/metabolism
MH  - Nerve Growth Factors/*metabolism
MH  - Neurons/cytology/*metabolism
MH  - Oligodendroglia/cytology/*metabolism
MH  - Physical Conditioning, Animal
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, trkB/*metabolism
MH  - Spinal Cord/cytology/metabolism
MH  - Time
MH  - Up-Regulation/physiology
EDAT- 2002/10/03 04:00
MHDA- 2002/10/18 04:00
CRDT- 2002/10/03 04:00
PHST- 2002/10/03 04:00 [pubmed]
PHST- 2002/10/18 04:00 [medline]
PHST- 2002/10/03 04:00 [entrez]
AID - S0014488602979434 [pii]
AID - 10.1006/exnr.2002.7943 [doi]
PST - ppublish
SO  - Exp Neurol. 2002 Aug;176(2):289-307. doi: 10.1006/exnr.2002.7943.