PMID- 11031087
OWN - NLM
STAT- MEDLINE
DCOM- 20001207
LR  - 20071114
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 166
IP  - 1
DP  - 2000 Nov
TI  - BDNF protects against spatial memory deficits following neonatal 
      hypoxia-ischemia.
PG  - 99-114
AB  - Hypoxic-ischemic (H-I) brain injury in the human perinatal period often leads to 
      significant long-term neurobehavioral dysfunction in the cognitive and 
      sensory-motor domains. Using a neonatal H-I injury model (unilateral carotid 
      ligation followed by hypoxia) in postnatal day seven rats, previous studies have 
      shown that neurotrophins, such as brain-derived neurotrophic factor (BDNF), can 
      be protective against neural tissue loss. The present study explored potential 
      relationships between neural protective and behavioral protective strategies in 
      this neonatal H-I model by determining if neonatal H-I was associated with 
      behavioral spatial learning and memory deficits and whether the neurotrophin BDNF 
      was protective against both brain injury and spatial learning/memory dysfunction. 
      Postnatal day seven rats received vehicle or BDNF pretreatments 
      (intracerebroventricular injections) followed by H-I or sham treatments and then 
      tested for spatial learning and memory on the simple place task in the Morris 
      water maze from postnatal days 20 to 30, and their brains were histologically 
      analyzed at 4 weeks following treatments. H-I rats with vehicle pretreatment 
      displayed significant tissue loss in the hippocampus (including CA1 neurons), 
      cortex, and striatum, as well as severe spatial memory deficits (e.g., short 
      probe times). BDNF pretreatment resulted in significant protection against both 
      H-I-induced brain tissue losses and spatial memory impairments. These findings 
      indicate that unilateral H-I brain injury in a neonatal rodent model is 
      associated with cognitive deficits, and that BDNF pretreatment is protective 
      against both brain injury and spatial memory impairment.
CI  - Copyright 2000 Academic Press.
FAU - Almli, C R
AU  - Almli CR
AD  - Department of Neurology, Washington University School of Medicine, St. Louis, 
      Missouri 63108-2212, USA.
FAU - Levy, T J
AU  - Levy TJ
FAU - Han, B H
AU  - Han BH
FAU - Shah, A R
AU  - Shah AR
FAU - Gidday, J M
AU  - Gidday JM
FAU - Holtzman, D M
AU  - Holtzman DM
LA  - eng
GR  - NS35902/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  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Animals, Newborn/*physiology
MH  - Asphyxia Neonatorum/*drug therapy/pathology/physiopathology
MH  - Brain/drug effects/pathology/physiopathology
MH  - Brain Injuries/drug therapy/pathology/physiopathology
MH  - Brain-Derived Neurotrophic Factor/metabolism/*pharmacology
MH  - Cell Count
MH  - Disease Models, Animal
MH  - Female
MH  - Humans
MH  - Hypoxia-Ischemia, Brain/*drug therapy/pathology/physiopathology
MH  - Infant, Newborn
MH  - Maze Learning/drug effects/physiology
MH  - Memory Disorders/*drug therapy/pathology/physiopathology
MH  - Nerve Degeneration/drug therapy/pathology/physiopathology
MH  - Pregnancy
MH  - Rats
MH  - Recovery of Function/drug effects/physiology
EDAT- 2000/10/14 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/10/14 11:00
PHST- 2000/10/14 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/10/14 11:00 [entrez]
AID - S0014-4886(00)97492-2 [pii]
AID - 10.1006/exnr.2000.7492 [doi]
PST - ppublish
SO  - Exp Neurol. 2000 Nov;166(1):99-114. doi: 10.1006/exnr.2000.7492.