PMID- 10456086
OWN - NLM
STAT- MEDLINE
DCOM- 19990909
LR  - 20191103
IS  - 1072-0502 (Print)
IS  - 1072-0502 (Linking)
VI  - 3
IP  - 2-3
DP  - 1996 Sep-Oct
TI  - The role of dendritic action potentials and Ca2+ influx in the induction of 
      homosynaptic long-term depression in hippocampal CA1 pyramidal neurons.
PG  - 160-9
AB  - Long-term depression (LTD) of synaptic efficacy at CA1 synapses is believed to be 
      a Ca(2+)-dependent process. We used high-speed fluorescence imaging and 
      patch-clamp techniques to quantify the spatial distribution of changes in 
      intracellular Ca2+ accompanying the induction of LTD at Schaffer collateral 
      synapses in CA1 pyramidal neurons. Low-frequency stimulation (3 Hz), which was 
      subthreshold for action potentials, produced small changes in [Ca2+]i and failed 
      to elicit LTD. Increasing the stimulus strength so that action potentials were 
      generated produced both robust LTD and increases in [Ca2+]i. Back-propagating 
      action potentials at 3 Hz in the absence of synaptic stimulation also produced 
      increases in [Ca2+]i, but failed to induce LTD. When subthreshold synaptic 
      stimulation was paired with back-propagating action potentials, however, large 
      increases in [Ca2+]i were observed and robust LTD was induced. The LTD was 
      blocked by the N-methyl-D-aspartate receptor (NMDAr) antagonist APV, and 
      stimulus-induced increases in [Ca2+]i were reduced throughout the neuron under 
      these conditions. The LTD was also dependent on Ca2+ influx via voltage-gated 
      Ca2+ channels (VGCCs), because LTD was severely attenuated or blocked by both 
      nimodipine and Ni2+. These findings suggest that back-propagating action 
      potentials can exert a powerful control over the induction of LTD and that both 
      VGCCs and NMDArs are involved in the induction of this form of plasticity.
FAU - Christie, B R
AU  - Christie BR
AD  - Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
FAU - Magee, J C
AU  - Magee JC
FAU - Johnston, D
AU  - Johnston D
LA  - eng
GR  - MH44754/MH/NIMH NIH HHS/United States
GR  - NS09882/NS/NINDS NIH HHS/United States
GR  - NS11535/NS/NINDS NIH HHS/United States
GR  - etc.
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  - Learn Mem
JT  - Learning & memory (Cold Spring Harbor, N.Y.)
JID - 9435678
RN  - 0 (Calcium Channels)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Action Potentials/physiology
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channels/physiology
MH  - Dendrites/*physiology
MH  - Electrophysiology
MH  - Hippocampus/cytology/*physiology
MH  - In Vitro Techniques
MH  - Ion Channel Gating/physiology
MH  - Long-Term Potentiation/*physiology
MH  - Pyramidal Cells/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/physiology
MH  - Synapses/*physiology
EDAT- 1996/09/01 00:00
MHDA- 1999/08/24 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1999/08/24 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
AID - 10.1101/lm.3.2-3.160 [doi]
PST - ppublish
SO  - Learn Mem. 1996 Sep-Oct;3(2-3):160-9. doi: 10.1101/lm.3.2-3.160.