PMID- 9582443
OWN - NLM
STAT- MEDLINE
DCOM- 19990105
LR  - 20190826
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 55
IP  - 2
DP  - 1998 Apr
TI  - Excitotoxic injury induces monocyte chemoattractant protein-1 expression in 
      neonatal rat brain.
PG  - 306-14
AB  - Intra-hippocampal injection of NMDA (12.5 nmol) in postnatal day 7 (P7) rats 
      results in neuronal necrosis and hippocampal atrophy; injury extends into the 
      adjacent striatum, thalamus and cortex. NMDA-induced injury is marked by an acute 
      microglial/monocyte response; the molecular signals that control this response 
      and the role of activated microglia/monocytes in the progression of excitotoxic 
      injury are unknown. Monocyte chemoattractant protein-1 (MCP-1) is a 
      well-characterized chemokine that regulates monocyte chemotaxis and activation, 
      and contributes to the pathogenesis of monocyte-dependent tissue injury in 
      several disease models. We hypothesized that MCP-1 could be a regulator of the 
      microglial/monocyte response to excitotoxic injury in neonatal rat brain. To 
      determine if intra-hippocampal NMDA injections induced MCP-1 mRNA expression, in 
      situ hybridization assays were performed in brain samples obtained from 7-day-old 
      rats, evaluated 0-24 h after intra-hippocampal NMDA injection. MCP-1 mRNA 
      expression was first detected at 2 h after lesioning, in the choroid fissure, 
      adjacent to the lesioned hippocampus; levels of expression increased markedly in 
      the lesioned hippocampus and adjacent structures within the first 16 h after NMDA 
      injection, and then rapidly declined. In control animals that received 
      intra-hippocampal saline injections, only minimal MCP-1 mRNA was detected, along 
      the injection track. These results demonstrate that excitotoxic injury 
      transiently induces MCP-1 gene expression in neonatal rat brain. The functional 
      role of MCP-1 in the injured brain remains to be determined.
CI  - Copyright 1998 Elsevier Science B.V.
FAU - Szaflarski, J
AU  - Szaflarski J
AD  - Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA.
FAU - Ivacko, J
AU  - Ivacko J
FAU - Liu, X H
AU  - Liu XH
FAU - Warren, J S
AU  - Warren JS
FAU - Silverstein, F S
AU  - Silverstein FS
LA  - eng
GR  - HL 48287/HL/NHLBI NIH HHS/United States
GR  - NS 31054/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lectins)
RN  - 0 (RNA, Messenger)
RN  - 6384-92-5 (N-Methylaspartate)
SB  - IM
MH  - Animals
MH  - Animals, Newborn/*metabolism
MH  - Brain/drug effects/*metabolism
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Hippocampus
MH  - Histocytochemistry
MH  - In Situ Hybridization
MH  - Injections
MH  - Lectins/metabolism
MH  - N-Methylaspartate/*toxicity
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 1998/06/24 00:00
MHDA- 1998/06/24 00:01
CRDT- 1998/06/24 00:00
PHST- 1998/06/24 00:00 [pubmed]
PHST- 1998/06/24 00:01 [medline]
PHST- 1998/06/24 00:00 [entrez]
AID - S0169328X98000138 [pii]
AID - 10.1016/s0169-328x(98)00013-8 [doi]
PST - ppublish
SO  - Brain Res Mol Brain Res. 1998 Apr;55(2):306-14. doi: 
      10.1016/s0169-328x(98)00013-8.