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Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

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Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
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Nuclear calcium signaling.

C Peter Bengtson1, Hilmar Bading

  • 1Department of Neurobiology, Interdisciplinary Centre for Neurosciences, University of Heidelberg, INF 364, 69120 Heidelberg, Germany. Bengtson@nbio.uni-heidelberg.de

Advances in Experimental Medicine and Biology
|February 22, 2012
PubMed
Summary
This summary is machine-generated.

Calcium signals link neuronal activity to gene expression, controlling synaptic plasticity and neuronal survival. This review explores how synaptic activity generates nuclear calcium signals for long-lasting changes in synaptic efficacy and memory.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Signaling

Background:

  • Calcium ions (Ca2+) are crucial intracellular messengers in neurons, mediating responses from synaptic activity to gene expression.
  • Synaptic activity triggers local calcium signaling cascades that regulate synaptic plasticity, including the insertion of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs).
  • Nuclear calcium signals, evoked by synaptic activity, regulate gene expression through pathways involving cAMP response element-binding protein (CREB) and CREB-binding protein (CBP).

Purpose of the Study:

  • To review the calcium signaling pathways involved in synaptically activated gene transcription.
  • To elucidate the physiological mechanisms by which synaptic activity evokes nuclear calcium signals.
  • To connect these calcium signaling events to long-lasting changes in synaptic efficacy and memory.

Main Methods:

  • Literature review of existing research on calcium signaling in neurons.
  • Analysis of studies investigating the role of various calcium channels and receptors (NMDARs, IP3Rs, VGCCs) in different neuronal compartments.
  • Synthesis of findings on the regulation of gene expression by nuclear calcium signals.

Main Results:

  • Distinct mechanisms mediate synaptically generated calcium signals in different neuronal compartments: NMDARs and ryanodine receptors in spines, IP3 receptors in dendrites, and L-type voltage-gated calcium channels (VGCCs) at the soma and nucleus.
  • Both NMDARs and IP3 receptors can contribute to somatic and nuclear calcium signals under specific conditions.
  • Synaptically evoked nuclear calcium signals regulate gene transcription, impacting neuronal function.

Conclusions:

  • Calcium signaling is a fundamental link between synaptic activity and gene expression, influencing neuronal plasticity, survival, and memory.
  • Understanding the compartmentalized mechanisms of calcium signaling is key to comprehending how synaptic activity leads to long-term neuronal changes.
  • This review highlights the critical role of nuclear calcium signals in translating transient synaptic events into enduring functional modifications.