PMID- 16822976
OWN - NLM
STAT- MEDLINE
DCOM- 20060725
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 26
IP  - 27
DP  - 2006 Jul 5
TI  - Altered balance of glutamatergic/GABAergic synaptic input and associated changes 
      in dendrite morphology after BDNF expression in BDNF-deficient hippocampal 
      neurons.
PG  - 7189-200
AB  - Cultured neurons from bdnf-/- mice display reduced densities of synaptic 
      terminals, although in vivo these deficits are small or absent. Here we aimed at 
      clarifying the local responses to postsynaptic brain-derived neurotrophic factor 
      (BDNF). To this end, solitary enhanced green fluorescent protein (EGFP)-labeled 
      hippocampal neurons from bdnf-/- mice were compared with bdnf-/- neurons after 
      transfection with BDNF, bdnf-/- neurons after transient exposure to exogenous 
      BDNF, and bdnf+/+ neurons in wild-type cultures. Synapse development was 
      evaluated on the basis of presynaptic immunofluorescence and whole-cell 
      patch-clamp recording of miniature postsynaptic currents. It was found that 
      neurons expressing BDNF::EGFP for at least 16 h attracted a larger number of 
      synaptic terminals than BDNF-deficient control neurons. Transfected BDNF formed 
      clusters in the vicinity of glutamatergic terminals and produced a stronger 
      upregulation of synaptic terminal numbers than high levels of ambient BDNF. 
      Glutamatergic and GABAergic synapses reacted differently to postsynaptic BDNF: 
      glutamatergic input increased, whereas GABAergic input decreased. 
      BDNF::EGFP-expressing neurons also differed from BDNF-deficient neurons in their 
      dendrite morphology: they exhibited weaker dendrite elongation and stronger 
      dendrite initiation. The upregulation of glutamatergic synaptic input and the 
      BDNF-induced downregulation of GABAergic synaptic terminal numbers by 
      postsynaptic BDNF depended on tyrosine receptor kinase B activity, as deduced 
      from the blocking effects of K252a. The suppression of dendrite elongation was 
      also prevented by block of tyrosine receptor kinase B but required, in addition, 
      glutamate receptor activity. Dendritic length decreased with the number of 
      glutamatergic contacts. These results illuminate the role of BDNF as a retrograde 
      synaptic regulator of synapse development and the dependence of dendrite 
      elongation on glutamatergic input.
FAU - Singh, B
AU  - Singh B
AD  - Developmental Physiology Group, Johannes Mueller Institute for Neurophysiology, 
      University Medical School (Charite) of the Humboldt University, D-10117 Berlin, 
      Germany.
FAU - Henneberger, C
AU  - Henneberger C
FAU - Betances, D
AU  - Betances D
FAU - Arevalo, M A
AU  - Arevalo MA
FAU - Rodriguez-Tebar, A
AU  - Rodriguez-Tebar A
FAU - Meier, J C
AU  - Meier JC
FAU - Grantyn, R
AU  - Grantyn R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
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)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
RN  - 62229-50-9 (Epidermal Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*physiology
MH  - Cells, Cultured
MH  - Dendrites/*physiology
MH  - Epidermal Growth Factor/genetics
MH  - Female
MH  - Gene Expression/physiology
MH  - Glutamic Acid/*physiology
MH  - Hippocampus/cytology/growth & development/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Neuronal Plasticity/physiology
MH  - Neurons/physiology/ultrastructure
MH  - Patch-Clamp Techniques
MH  - Pregnancy
MH  - Receptor, Nerve Growth Factor/physiology
MH  - Receptor, trkB/physiology
MH  - Synapses/*physiology
MH  - Transfection
MH  - gamma-Aminobutyric Acid/*physiology
PMC - PMC6673958
EDAT- 2006/07/11 09:00
MHDA- 2006/07/26 09:00
PMCR- 2007/01/05
CRDT- 2006/07/11 09:00
PHST- 2006/07/11 09:00 [pubmed]
PHST- 2006/07/26 09:00 [medline]
PHST- 2006/07/11 09:00 [entrez]
PHST- 2007/01/05 00:00 [pmc-release]
AID - 26/27/7189 [pii]
AID - 10.1523/JNEUROSCI.5474-05.2006 [doi]
PST - ppublish
SO  - J Neurosci. 2006 Jul 5;26(27):7189-200. doi: 10.1523/JNEUROSCI.5474-05.2006.