PMID- 17546681
OWN - NLM
STAT- MEDLINE
DCOM- 20071031
LR  - 20211203
IS  - 1050-9631 (Print)
IS  - 1050-9631 (Linking)
VI  - 17
IP  - 8
DP  - 2007
TI  - Perinatal iron deficiency results in altered developmental expression of genes 
      mediating energy metabolism and neuronal morphogenesis in hippocampus.
PG  - 679-91
AB  - The human and rat hippocampus is highly susceptible to iron deficiency (ID) 
      during the late fetal, early neonatal time period which is a peak time of 
      regulated brain iron uptake and utilization. ID during this period alters 
      cognitive development and is characterized by distinctive, long-term changes in 
      hippocampal cellular growth and function. The fundamental processes underlying 
      these changes are not entirely understood. In this study, ID-induced changes in 
      expression of 25 genes implicated in iron metabolism, including cell growth and 
      energy metabolism, dendrite morphogenesis, and synaptic connectivity were 
      assessed from postnatal day (P) 7 to P65 in hippocampus. All 25 genes showed 
      altered expression during the period of ID (P7, 15, and 30); 10 had changes on 
      P65 after iron repletion. ID caused long-term diminished protein levels of four 
      factors critical for hippocampal neuron differentiation and plasticity, including 
      CamKII alpha, Fkbp1a (Fkbp12), Dlgh4 (PSD-95), and Vamp1 (Synaptobrevin-1). ID 
      altered gene expression in the mammalian target of rapamycin (mTOR) pathway and 
      in a gene network implicated in Alzheimer disease etiology. ID during late fetal 
      and early postnatal life alters the levels and timing of expression of critical 
      genes involved in hippocampal development and function. The study provides 
      targets for future studies in elucidating molecular mechanisms underpinning 
      iron's role in cognitive development and function.
CI  - (c) 2007 Wiley-Liss, Inc.
FAU - Carlson, Erik S
AU  - Carlson ES
AD  - Medical Scientist Training Program, Department of Pediatrics, University of 
      Minnesota, Minneapolis, Minnesota, USA.
FAU - Stead, John D H
AU  - Stead JD
FAU - Neal, Charles R
AU  - Neal CR
FAU - Petryk, Anna
AU  - Petryk A
FAU - Georgieff, Michael K
AU  - Georgieff MK
LA  - eng
GR  - F31 NS047876/NS/NINDS NIH HHS/United States
GR  - 1F31-NS047876/NS/NINDS NIH HHS/United States
GR  - R01 HD-29421/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Hippocampus
JT  - Hippocampus
JID - 9108167
RN  - E1UOL152H7 (Iron)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - *Cell Size
MH  - Disease Models, Animal
MH  - Energy Metabolism/*physiology
MH  - Female
MH  - Gene Expression Profiling/methods
MH  - Gene Expression Regulation, Developmental/drug effects/*physiology
MH  - Hippocampus/*pathology
MH  - Iron/pharmacology
MH  - *Iron Deficiencies
MH  - *Iron Metabolism Disorders/metabolism/pathology/physiopathology
MH  - Male
MH  - Neurons/*cytology
MH  - Oligonucleotide Array Sequence Analysis/methods
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
EDAT- 2007/06/05 09:00
MHDA- 2007/11/01 09:00
CRDT- 2007/06/05 09:00
PHST- 2007/06/05 09:00 [pubmed]
PHST- 2007/11/01 09:00 [medline]
PHST- 2007/06/05 09:00 [entrez]
AID - 10.1002/hipo.20307 [doi]
PST - ppublish
SO  - Hippocampus. 2007;17(8):679-91. doi: 10.1002/hipo.20307.