PMID- 10684880
OWN - NLM
STAT- MEDLINE
DCOM- 20000309
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 20
IP  - 5
DP  - 2000 Mar 1
TI  - NMDA receptor-mediated subthreshold Ca(2+) signals in spines of hippocampal 
      neurons.
PG  - 1791-9
AB  - We have used rapid confocal microscopy to investigate the mechanism of Ca(2+) 
      signals in individual dendritic spines of hippocampal CA1 pyramidal cells. The 
      experiments focused on the signals that occur during single weak synaptic 
      responses that were subthreshold for triggering postsynaptic action potentials. 
      These Ca(2+) signals were not strongly affected by blocking the EPSPs with the 
      AMPA receptor antagonist CNQX. The signals were also not strongly reduced by 
      blocking T-type voltage-gated Ca(2+) channels (VGCCs) with Ni(2+) or by blocking 
      a broad range of VGCCs with intracellular D890. The spine Ca(2+) signals were 
      blocked by NMDA receptor channel (NMDAR) antagonist and had the voltage 
      dependence characteristic of these channels. Neither ryanodine nor cyclopiazonic 
      acid (CPA), substances known to deplete intracellular Ca(2+) stores, 
      substantially reduced the amplitude of synaptically evoked Ca(2+) signals. CPA 
      slowed the recovery phase of Ca(2+) signals in spines produced by synaptic 
      stimulation or by backpropagating action potentials, suggesting a role of 
      intracellular stores in Ca(2+) reuptake. Thus, we find that Ca(2+) release from 
      intracellular stores is not required to produce spine Ca(2+) signals. We conclude 
      that synaptic Ca(2+) signals in spines are primarily caused by Ca(2+) entry 
      through NMDARs. Although these channels are largely blocked by Mg(2+) at voltages 
      near the resting potential, they can nevertheless produce significant Ca(2+) 
      elevation. The resulting Ca(2+) signals are an integral component of individual 
      evoked or spontaneous synaptic events and may be important in the maintenance of 
      synaptic function.
FAU - Kovalchuk, Y
AU  - Kovalchuk Y
AD  - Physiologisches Institut, Universitat des Saarlandes, 66421 Homburg, Germany.
FAU - Eilers, J
AU  - Eilers J
FAU - Lisman, J
AU  - Lisman J
FAU - Konnerth, A
AU  - Konnerth A
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 (Calcium Channels, T-Type)
RN  - 0 (Dinucleoside Phosphates)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 15662-33-6 (Ryanodine)
RN  - 2382-66-3 (cytidylyl adenosine)
RN  - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
RN  - 76726-92-6 (2-Amino-5-phosphonovalerate)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - 2-Amino-5-phosphonovalerate/pharmacology
MH  - 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology
MH  - Animals
MH  - Calcium/metabolism
MH  - Calcium Channels, T-Type/physiology
MH  - Calcium Signaling/drug effects/*physiology
MH  - Cells, Cultured
MH  - Dendrites/chemistry/*physiology
MH  - Dinucleoside Phosphates/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Hippocampus/*cytology
MH  - Membrane Potentials/drug effects/physiology
MH  - Microscopy, Confocal
MH  - Pyramidal Cells/physiology/ultrastructure
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, AMPA/physiology
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
MH  - Ryanodine/pharmacology
PMC - PMC6772937
EDAT- 2000/02/24 00:00
MHDA- 2000/03/11 00:00
PMCR- 2000/09/01
CRDT- 2000/02/24 00:00
PHST- 2000/02/24 00:00 [pubmed]
PHST- 2000/03/11 00:00 [medline]
PHST- 2000/02/24 00:00 [entrez]
PHST- 2000/09/01 00:00 [pmc-release]
AID - 3936 [pii]
AID - 10.1523/JNEUROSCI.20-05-01791.2000 [doi]
PST - ppublish
SO  - J Neurosci. 2000 Mar 1;20(5):1791-9. doi: 10.1523/JNEUROSCI.20-05-01791.2000.