PMID- 18440495
OWN - NLM
STAT- MEDLINE
DCOM- 20080826
LR  - 20080521
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1212
DP  - 2008 May 30
TI  - Degenerative alterations in the visual pathway after NMDA-induced retinal damage 
      in mice.
PG  - 89-101
LID - 10.1016/j.brainres.2008.03.021 [doi]
AB  - In the present study, intravitreal injection of N-methyl-d-aspartate (NMDA) into 
      the left eye induced retinal damage (decreases in the number of retinal ganglion 
      cells) at 1 day after the injection. At 7 days after the injection, atrophy of 
      the optic tract was observed on the contralateral side, but not on the 
      ipsilateral side. Number of neuronal nuclear specific protein 
      (NeuN)-immunostained neurons were decreased in the contralateral dorsal LGN 
      (dLGN) and contralateral ventral LGN-lateral (vLGN-l) at 90 and 180 days, 
      respectively, after the injection. Furthermore, expressions of glial fibrillary 
      acid protein (GFAP) were increased in the contralateral dLGN and contralateral 
      vLGN-l at 7 and 30 days, respectively, and those of brain-derived neurotrophic 
      factor (BDNF) were increased in the contralateral dLGN at 30 and 90 days and in 
      the contralateral vLGN-l at 7 and 30 days. All NeuN-positive neuronal cells 
      exhibited BDNF, whereas only some GFAP-positive astroglial cells exhibited BDNF. 
      However, the contralateral ventral LGN-medial (vLGN-m) and ipsilateral LGN 
      displayed no significant differences related to NeuN, GFAP, or BDNF 
      immunohistochemistry. Taken together, these results indicate that time-dependent 
      alterations occurred after the NMDA injection along the retinogeniculate pathway 
      (from retina to LGN), and that the degree of damage in the LGN was 
      region-dependent. In addition, the increased activated astroglial cells and 
      expressions of BDNF in the damaged regions may play some roles in the 
      cell-survival process of the LGN.
FAU - Ito, Yasushi
AU  - Ito Y
AD  - Department of Biofunctional Evaluation, Molecular Pharmacology, Gifu 
      Pharmaceutical University, 5-6-1 Mitahora-higashi, Gifu 502-8585, Japan.
FAU - Shimazawa, Masamitsu
AU  - Shimazawa M
FAU - Inokuchi, Yuta
AU  - Inokuchi Y
FAU - Fukumitsu, Hidefumi
AU  - Fukumitsu H
FAU - Furukawa, Syouei
AU  - Furukawa S
FAU - Araie, Makoto
AU  - Araie M
FAU - Hara, Hideaki
AU  - Hara H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080321
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - EC 4.2.1.11 (Phosphopyruvate Hydratase)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Functional Laterality
MH  - Gene Expression Regulation/physiology
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - *N-Methylaspartate
MH  - Nerve Degeneration/*etiology
MH  - Neurons/metabolism/pathology
MH  - Phosphopyruvate Hydratase/metabolism
MH  - *Retinal Diseases/chemically induced/complications/pathology
MH  - Time Factors
MH  - Visual Pathways/*pathology
EDAT- 2008/04/29 09:00
MHDA- 2008/08/30 09:00
CRDT- 2008/04/29 09:00
PHST- 2007/12/04 00:00 [received]
PHST- 2008/03/05 00:00 [revised]
PHST- 2008/03/05 00:00 [accepted]
PHST- 2008/04/29 09:00 [pubmed]
PHST- 2008/08/30 09:00 [medline]
PHST- 2008/04/29 09:00 [entrez]
AID - S0006-8993(08)00618-5 [pii]
AID - 10.1016/j.brainres.2008.03.021 [doi]
PST - ppublish
SO  - Brain Res. 2008 May 30;1212:89-101. doi: 10.1016/j.brainres.2008.03.021. Epub 
      2008 Mar 21.