PMID- 17610571
OWN - NLM
STAT- MEDLINE
DCOM- 20070824
LR  - 20131121
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 25
IP  - 12
DP  - 2007 Jun
TI  - AAV-mediated delivery of BDNF augments neurogenesis in the normal and quinolinic 
      acid-lesioned adult rat brain.
PG  - 3513-25
AB  - Brain-derived neurotrophic factor (BDNF) plays a major role in regulating the 
      survival and fate of progenitor cells in the adult brain. In order to extend 
      previous observations in the normal adult brain and advance our knowledge 
      regarding the effect of BDNF on neurogenesis in the injured brain, this study 
      directly compared the effect of BDNF on basal and injury-induced neurogenesis in 
      relation to progenitor cell distribution and levels of neuronal differentiation 
      and survival. BDNF was overexpressed in the subventricular zone (SVZ) via 
      recombinant adeno-associated virus (AAV(1/2)) delivery, and newly generated cells 
      were identified using bromodeoxyuridine (BrdU) labelling. Selective striatal cell 
      loss was induced in a subgroup of rats by unilateral striatal injection of 
      quinolinic acid (QA) 21 days after AAV(1/2) injection. In the normal brain, BDNF 
      overexpression significantly increased BrdU-positive cell numbers in the rostral 
      migratory stream, indicating enhanced progenitor cell migration. Following QA 
      lesioning, we observed a reduction in BrdU immunoreactivity in the SVZ. 
      Overexpression of BDNF restored BrdU-positive cell numbers in the QA-lesioned SVZ 
      to that observed in the normal brain. Most significantly, BDNF enhanced the 
      recruitment of progenitor cells to the QA-lesioned striatum and promoted neuronal 
      differentiation in both the normal and QA-lesioned striatum. Our findings 
      indicate that BDNF augments the recruitment, neuronal differentiation and 
      survival of progenitor cells in both neurogenic and non-neurogenic regions of the 
      normal or QA-lesioned brain. Enhanced expression of BDNF may therefore be a 
      viable strategy for augmenting neurogenesis from endogenous progenitor cells.
FAU - Henry, Rebecca A
AU  - Henry RA
AD  - Department of Pharmacology and Clinical Pharmacology, University of Auckland, 
      Private Bag 92019, Auckland, New Zealand.
FAU - Hughes, Stephanie M
AU  - Hughes SM
FAU - Connor, Bronwen
AU  - Connor B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Tissue Proteins)
RN  - F6F0HK1URN (Quinolinic Acid)
RN  - G34N38R2N1 (Bromodeoxyuridine)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Brain Injuries/chemically induced/*pathology/*physiopathology/therapy
MH  - Brain-Derived Neurotrophic Factor/administration & dosage/*metabolism
MH  - Bromodeoxyuridine/metabolism
MH  - Cell Count/methods
MH  - Cell Differentiation/drug effects/physiology
MH  - Cerebral Ventricles/drug effects/pathology
MH  - Dependovirus/*physiology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Male
MH  - Nerve Tissue Proteins/metabolism
MH  - Neurons/drug effects/*physiology
MH  - Quinolinic Acid
MH  - Rats
MH  - Rats, Wistar
MH  - Stem Cells/drug effects/*physiology
EDAT- 2007/07/06 09:00
MHDA- 2007/08/25 09:00
CRDT- 2007/07/06 09:00
PHST- 2007/07/06 09:00 [pubmed]
PHST- 2007/08/25 09:00 [medline]
PHST- 2007/07/06 09:00 [entrez]
AID - EJN5625 [pii]
AID - 10.1111/j.1460-9568.2007.05625.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2007 Jun;25(12):3513-25. doi: 10.1111/j.1460-9568.2007.05625.x.