PMID- 17110740
OWN - NLM
STAT- MEDLINE
DCOM- 20070117
LR  - 20061119
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 96
IP  - 6
DP  - 2006 Dec
TI  - Presynaptic plasticity in an immature neocortical network requires NMDA receptor 
      activation and BDNF release.
PG  - 3512-6
AB  - Activity-dependent developmental maturation of the neocortical network is thought 
      to involve the stabilization and potentiation of immature synapses. In 
      particular, N-methyl-d-aspartate (NMDA) receptor-dependent long-term plasticity 
      that is expressed presynaptically appears to be crucial for the selection of 
      functionally adequate synapses. However, presynaptic expression of long-term 
      plasticity in neocortical neurons has mainly been studied indirectly by 
      electrophysiological techniques. Here we analyzed presynaptic plasticity directly 
      by repeated imaging of actively cycling presynaptic vesicles with the styryl dye 
      FM4-64 in cultured neocortical neurons at 34 degrees C. To monitor long-term 
      changes, stimulation-induced saturating FM4-64 staining and subsequent destaining 
      was performed twice with an interval of 1.5 h between stainings and with the 
      first staining serving as a plasticity stimulus. In the vast majority of 
      presynaptic release sites, we found an increase in the mean fluorescence 
      intensity after the second staining indicating an enhanced number of cycling 
      synaptic vesicles. Most intriguingly, we additionally observed the appearance of 
      new active release sites. As demonstrated by the addition of the NMDA receptor 
      antagonist d-2-amino-5-phosphonopentanoic acid (d-AP5), both plasticity phenomena 
      were strictly dependent on NMDA receptor activation. This suggests that a 
      subpopulation of release sites was functionally silent during the first round of 
      staining. Moreover, we studied a potential role of brain-derived neurotrophic 
      factor (BDNF) in this type of presynaptic plasticity by imaging BDNF-deficient 
      neocortical neurons. The increase in fluorescence intensity was strongly 
      inhibited in BDNF-knockout neurons and was absent in wild-type neurons in the 
      presence of BDNF scavenging trkB receptor bodies. These results indicate that 
      BDNF might play an important role as a plasticity-related messenger molecule in 
      neocortical neurons.
FAU - Walz, Corinna
AU  - Walz C
AD  - Institut fur Neuro- und Sinnesphysiologie, Heinrich-Heine-Universitat Dusseldorf, 
      Universitatsstrasse 1, D-40225 Dusseldorf, Germany.
FAU - Jungling, Kay
AU  - Jungling K
FAU - Lessmann, Volkmar
AU  - Lessmann V
FAU - Gottmann, Kurt
AU  - Gottmann K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Coloring Agents)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (FM1 43)
RN  - 0 (Pyridinium Compounds)
RN  - 0 (Quaternary Ammonium Compounds)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Receptors, Presynaptic)
RN  - 76726-92-6 (2-Amino-5-phosphonovalerate)
SB  - IM
MH  - 2-Amino-5-phosphonovalerate/pharmacology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Cells, Cultured
MH  - Coloring Agents
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Female
MH  - Mice
MH  - Mice, Knockout
MH  - Neocortex/cytology/metabolism/*physiology
MH  - Nerve Net/*physiology
MH  - Neuronal Plasticity/*physiology
MH  - Pregnancy
MH  - Pyridinium Compounds
MH  - Quaternary Ammonium Compounds
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology
MH  - Receptors, Presynaptic/*physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Spectrometry, Fluorescence
EDAT- 2006/11/18 09:00
MHDA- 2007/01/18 09:00
CRDT- 2006/11/18 09:00
PHST- 2006/11/18 09:00 [pubmed]
PHST- 2007/01/18 09:00 [medline]
PHST- 2006/11/18 09:00 [entrez]
AID - 96/6/3512 [pii]
AID - 10.1152/jn.00018.2006 [doi]
PST - ppublish
SO  - J Neurophysiol. 2006 Dec;96(6):3512-6. doi: 10.1152/jn.00018.2006.