PMID- 10986348
OWN - NLM
STAT- MEDLINE
DCOM- 20001214
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 877
IP  - 2
DP  - 2000 Sep 22
TI  - Infarct tolerance accompanied enhanced BDNF-like immunoreactivity in neuronal 
      nuclei.
PG  - 331-44
AB  - A prolonged period (48 h) of cortical spreading depression (CSD) induced 
      resistance against severe focal cerebral ischemia (infarct tolerance), however, 
      the mechanism behind this is unknown. The infarct tolerance was a transient 
      phenomenon; the resistance increased linearly for the initial 12 days, peaking 
      from 12 to 15 days after a preconditioning of CSD, and was decreased thereafter. 
      This study examined the time course of brain-derived neurotrophic factor (BDNF), 
      heat shock protein (hsp)27 and 70, and glial fibrillary acidic protein (GFAP) 
      expressions after CSD in the brain. Immunohistochemical expression of BDNF, 
      hsp27, hsp70, or GFAP following a prolonged period of CSD induced by 
      KCl-infusion, or following NaCl-infusion was analyzed by regional densitometry 
      for 24 days in the rat neocortex. In addition, BDNF protein was measured 
      quantitatively by two-site ELISA assay in the neocortex (n=6 at each time point). 
      The GFAP expression was elevated in astrocytes (compared to the normal level of 
      immunodensity) during the period peaking on day 3-6 following the CSD. The hsp27 
      immunoreactivity was also elevated in astrocytes from day 1 to 12 peaking on day 
      1 and 6, but there was no expression of hsp70 during the period following CSD. 
      The immunoreactivity for BDNF was elevated in neurons from day 0 to 18 peaking on 
      day 1 and 6. The protein levels of BDNF in the neocortex were significantly 
      elevated from day 0 to 12 peaking on days 0 and 6 (compared to the normal level) 
      (P<0.05). Using a laser-scanning confocal imaging system, the BDNF-like 
      immunoreactivity in neuronal nuclei was found to increase linearly peaking on day 
      12, which correlated well with the development of infarct tolerance. The 
      intranuclear increase in BDNF-like protein might contribute to the induction of 
      infarct tolerance in the brain.
FAU - Yanamoto, H
AU  - Yanamoto H
AD  - National Cardio-Vascular Center and NCVC Research Institute, 5-7-1 Fujishiro-dai, 
      Suita, Osaka 565-8565, Japan. yanamoto@ri.ncvc.go.jp
FAU - Mizuta, I
AU  - Mizuta I
FAU - Nagata, I
AU  - Nagata I
FAU - Xue, J
AU  - Xue J
FAU - Zhang, Z
AU  - Zhang Z
FAU - Kikuchi, H
AU  - Kikuchi H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (HSP70 Heat-Shock Proteins)
RN  - 0 (Heat-Shock Proteins)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 660YQ98I10 (Potassium Chloride)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism/pathology
MH  - Brain/*metabolism/pathology/physiopathology
MH  - Brain Infarction/*metabolism/pathology/physiopathology
MH  - Brain Ischemia/*metabolism/pathology/*physiopathology
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cortical Spreading Depression/drug effects/*physiology
MH  - Densitometry
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - HSP70 Heat-Shock Proteins/metabolism
MH  - Heat-Shock Proteins/metabolism
MH  - Immunohistochemistry
MH  - Male
MH  - Microscopy, Confocal
MH  - Neurons/*metabolism/pathology
MH  - Potassium Chloride/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium Chloride/pharmacology
MH  - Time Factors
EDAT- 2000/09/15 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/09/15 11:00
PHST- 2000/09/15 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/09/15 11:00 [entrez]
AID - S0006899300027189 [pii]
AID - 10.1016/s0006-8993(00)02718-9 [doi]
PST - ppublish
SO  - Brain Res. 2000 Sep 22;877(2):331-44. doi: 10.1016/s0006-8993(00)02718-9.