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A Calcium-Dependent Mechanism of Neuronal Memory.

Gasque G - PLoS Biol. (2015)

Bottom Line: A neuron's record of its previous activity underlies animal memory.A new study reveals a role for the release of calcium ions from intracellular stores in mediating spatially compartmentalized memory of the activity history of a neuron.

View Article: PubMed Central - PubMed

Affiliation: Public Library of Science, San Francisco, California, United States of America.

ABSTRACT
A neuron's record of its previous activity underlies animal memory. A new study reveals a role for the release of calcium ions from intracellular stores in mediating spatially compartmentalized memory of the activity history of a neuron.

No MeSH data available.


A new mechanism of storing patterns of previous neuronal activity: back-propagating action potentials activate voltage-gated Ca2+ channels (VGCCs) and ryanodine receptor (RyR) intracellular Ca2+ release channels; spine-specific Ca2+ memory is the result of Ca2+ release from intracellular stores via ryanodine receptors.AP, action potential. Image credit: Friedrich Johenning, Ulrike Pannasch, and Dietmar Schmitz.
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pbio.1002182.g001: A new mechanism of storing patterns of previous neuronal activity: back-propagating action potentials activate voltage-gated Ca2+ channels (VGCCs) and ryanodine receptor (RyR) intracellular Ca2+ release channels; spine-specific Ca2+ memory is the result of Ca2+ release from intracellular stores via ryanodine receptors.AP, action potential. Image credit: Friedrich Johenning, Ulrike Pannasch, and Dietmar Schmitz.

Mentions: When a neuron gets activated, it fires an action potential, a short-lasting change in membrane potential that travels unidirectionally from near the cell body to the axon terminal, where it triggers the release of a chemical signal—a neurotransmitter—into the synaptic cleft, to be sensed by the adjacent neuron. However, action potentials also propagate back to the cell body and the dendrites of neurons. Johenning, Theis, and colleagues demonstrated that back-propagating action potentials are not only coupled to the activation of voltage-gated Ca2+ channels in the plasma membrane of the dendritic spine but also to the release of Ca2+ from intracellular stores via ryanodine receptors. More importantly, their study shows that when a dendritic spine sees a short burst of action potentials—similar to patterns of activity seen in freely moving animals—the Ca2+ transients elicited by subsequent back-propagating action potentials are enhanced for several minutes after the burst. These results indicate that the neuron can “remember” its previous history of activity and express this memory as a sustained increase in the amplitude of Ca2+ transients in a spine-specific manner (Fig 1).


A Calcium-Dependent Mechanism of Neuronal Memory.

Gasque G - PLoS Biol. (2015)

A new mechanism of storing patterns of previous neuronal activity: back-propagating action potentials activate voltage-gated Ca2+ channels (VGCCs) and ryanodine receptor (RyR) intracellular Ca2+ release channels; spine-specific Ca2+ memory is the result of Ca2+ release from intracellular stores via ryanodine receptors.AP, action potential. Image credit: Friedrich Johenning, Ulrike Pannasch, and Dietmar Schmitz.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4476717&req=5

pbio.1002182.g001: A new mechanism of storing patterns of previous neuronal activity: back-propagating action potentials activate voltage-gated Ca2+ channels (VGCCs) and ryanodine receptor (RyR) intracellular Ca2+ release channels; spine-specific Ca2+ memory is the result of Ca2+ release from intracellular stores via ryanodine receptors.AP, action potential. Image credit: Friedrich Johenning, Ulrike Pannasch, and Dietmar Schmitz.
Mentions: When a neuron gets activated, it fires an action potential, a short-lasting change in membrane potential that travels unidirectionally from near the cell body to the axon terminal, where it triggers the release of a chemical signal—a neurotransmitter—into the synaptic cleft, to be sensed by the adjacent neuron. However, action potentials also propagate back to the cell body and the dendrites of neurons. Johenning, Theis, and colleagues demonstrated that back-propagating action potentials are not only coupled to the activation of voltage-gated Ca2+ channels in the plasma membrane of the dendritic spine but also to the release of Ca2+ from intracellular stores via ryanodine receptors. More importantly, their study shows that when a dendritic spine sees a short burst of action potentials—similar to patterns of activity seen in freely moving animals—the Ca2+ transients elicited by subsequent back-propagating action potentials are enhanced for several minutes after the burst. These results indicate that the neuron can “remember” its previous history of activity and express this memory as a sustained increase in the amplitude of Ca2+ transients in a spine-specific manner (Fig 1).

Bottom Line: A neuron's record of its previous activity underlies animal memory.A new study reveals a role for the release of calcium ions from intracellular stores in mediating spatially compartmentalized memory of the activity history of a neuron.

View Article: PubMed Central - PubMed

Affiliation: Public Library of Science, San Francisco, California, United States of America.

ABSTRACT
A neuron's record of its previous activity underlies animal memory. A new study reveals a role for the release of calcium ions from intracellular stores in mediating spatially compartmentalized memory of the activity history of a neuron.

No MeSH data available.