PMID- 10559430
OWN - NLM
STAT- MEDLINE
DCOM- 20000621
LR  - 20181113
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 22
DP  - 1999 Nov 15
TI  - Brain-derived neurotrophic factor overexpression induces precocious critical 
      period in mouse visual cortex.
PG  - RC40
AB  - Brain-derived neurotrophic factor (BDNF) is a candidate molecule for regulating 
      activity-dependent synaptic plasticity on the grounds of its expression pattern 
      in developing visual cortex and that of its receptor, trkB (Castr inverted question markn et al., 1992; 
      Bozzi et al., 1995; Schoups et al., 1995; Cabelli et al., 1996), as well as the 
      modulation of these patterns by activity (Castr inverted question markn et al., 1992; Bozzi et al., 
      1995; Schoups et al., 1995). Infusing trkB ligands or their neutralizing agents, 
      the trkB-IgG fusion proteins, into visual cortex alters the development and 
      plasticity of ocular dominance columns (Cabelli et al., 1995; Riddle et al., 
      1995; Galuske et al., 1996 ; Gillespie et al., 1996; Cabelli et al., 1997). To 
      test further the physiological role of BDNF, we studied a transgenic mouse that 
      expresses elevated levels of BDNF in primary visual cortex (V1) postnatally 
      (Huang et al., 1999). We found that unlike the infusion experiments, excess BDNF 
      expressed in mouse visual cortex did not block ocular dominance plasticity. 
      Instead, single neurons in V1 of the BDNF transgenic mice were as susceptible to 
      the effects of monocular deprivation (MD) as neurons in wild-type mice, but only 
      during a precocious critical period. At a time when V1 in the wild-type mouse 
      responded maximally to a 4 d MD with a reduction in its response to deprived eye 
      visual stimulation, the transgenic mouse V1 had already passed the peak of its 
      precocious critical period and no longer responded maximally. This finding 
      suggests a role for BDNF in promoting the postnatal maturation of cortical 
      circuitry.
FAU - Hanover, J L
AU  - Hanover JL
AD  - Neuroscience Graduate Program and Department of Physiology, University of 
      California, San Francisco, California 94143, USA.
FAU - Huang, Z J
AU  - Huang ZJ
FAU - Tonegawa, S
AU  - Tonegawa S
FAU - Stryker, M P
AU  - Stryker MP
LA  - eng
GR  - NS32925/NS/NINDS NIH HHS/United States
GR  - P01 NS016033-190017/NS/NINDS NIH HHS/United States
GR  - NS16033/NS/NINDS NIH HHS/United States
GR  - R01 NS032925/NS/NINDS NIH HHS/United States
GR  - P01 NS016033/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  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism/physiology
MH  - Evoked Potentials, Visual/physiology
MH  - Mice
MH  - Neuronal Plasticity/*physiology
MH  - Visual Cortex/*metabolism/*physiology
PMC - PMC2424259
MID - NIHMS50192
EDAT- 1999/11/13 00:00
MHDA- 2000/06/24 00:00
PMCR- 2000/05/15
CRDT- 1999/11/13 00:00
PHST- 1999/11/13 00:00 [pubmed]
PHST- 2000/06/24 00:00 [medline]
PHST- 1999/11/13 00:00 [entrez]
PHST- 2000/05/15 00:00 [pmc-release]
AID - 3687 [pii]
AID - 10.1523/JNEUROSCI.19-22-j0003.1999 [doi]
PST - ppublish
SO  - J Neurosci. 1999 Nov 15;19(22):RC40. doi: 10.1523/JNEUROSCI.19-22-j0003.1999.