PMID- 11567081
OWN - NLM
STAT- MEDLINE
DCOM- 20011011
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 21
IP  - 19
DP  - 2001 Oct 1
TI  - Postsynaptic depolarization scales quantal amplitude in cortical pyramidal 
      neurons.
PG  - RC170
AB  - Pyramidal neurons scale the strength of all of their excitatory synapses up or 
      down in response to long-term changes in activity, and in the direction needed to 
      stabilize firing rates. This form of homeostatic plasticity is likely to play an 
      important role in stabilizing firing rates during learning and developmental 
      plasticity, but the signals that translate a change in activity into global 
      changes in synaptic strength are poorly understood. Some but not all of the 
      effects of long-lasting changes in activity on synaptic strengths can be 
      accounted for by activity-dependent release of the neurotrophin brain-derived 
      neurotrophic factor (BDNF). Other candidate activity signals include changes in 
      glutamate receptor (GluR) activation, changes in firing rate, or changes in the 
      average level of postsynaptic depolarization. Here we combined elevated KCl (3-12 
      mm) with ionotropic receptor blockade to dissociate postsynaptic depolarization 
      from receptor activation. Chronic (48 hr) depolarization, ranging between -62 and 
      -36 mV, parametrically reduced the quantal amplitude of excitatory synapses in a 
      BDNF-independent manner. This effect of depolarization did not depend on AMPA, 
      NMDA, or GABA(A) receptor signaling, action-potential generation, or metabotropic 
      GluR activation. Together with previous work, these data suggest that there are 
      two independent signals that regulate activity-dependent synaptic scaling in 
      pyramidal neurons: low levels of BDNF cause excitatory synapses to scale up in 
      strength, whereas depolarization causes excitatory synapses to scale down in 
      strength.
FAU - Leslie, K R
AU  - Leslie KR
AD  - Department of Biology and Center for Complex Systems, Brandeis University, 
      Waltham, Massachusetts 02454, USA.
FAU - Nelson, S B
AU  - Nelson SB
FAU - Turrigiano, G G
AU  - Turrigiano GG
LA  - eng
GR  - K02 NS01893/NS/NINDS NIH HHS/United States
GR  - R01 NS36853/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
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)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels, L-Type)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (GABA Antagonists)
RN  - 0 (GABA-A Receptor Antagonists)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 660YQ98I10 (Potassium Chloride)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Action Potentials/drug effects/physiology
MH  - Animals
MH  - Astrocytes/cytology
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels, L-Type/metabolism
MH  - Cells, Cultured
MH  - Cerebral Cortex/cytology/drug effects/*physiology
MH  - Coculture Techniques
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - GABA Antagonists/pharmacology
MH  - GABA-A Receptor Antagonists
MH  - Membrane Potentials/drug effects/physiology
MH  - Neuronal Plasticity/drug effects/physiology
MH  - Patch-Clamp Techniques
MH  - Potassium Chloride/pharmacology
MH  - Pyramidal Cells/drug effects/*physiology
MH  - Rats
MH  - Receptor, trkB/antagonists & inhibitors
MH  - Receptors, Metabotropic Glutamate/antagonists & inhibitors/metabolism
MH  - Signal Transduction/drug effects
MH  - Synapses/drug effects/*physiology
PMC - PMC6762907
EDAT- 2001/09/22 10:00
MHDA- 2001/10/12 10:01
PMCR- 2002/04/01
CRDT- 2001/09/22 10:00
PHST- 2001/09/22 10:00 [pubmed]
PHST- 2001/10/12 10:01 [medline]
PHST- 2001/09/22 10:00 [entrez]
PHST- 2002/04/01 00:00 [pmc-release]
AID - 20015671 [pii]
AID - 5671 [pii]
AID - 10.1523/JNEUROSCI.21-19-j0005.2001 [doi]
PST - ppublish
SO  - J Neurosci. 2001 Oct 1;21(19):RC170. doi: 10.1523/JNEUROSCI.21-19-j0005.2001.