Rapid, synaptically driven increases in the intrinsic excitability of cerebellar deep nuclear neurons

Aizenman, Carlos D.; Linden, David J.

doi:10.1038/72049

Cited by 247 publications

(234 citation statements)

References 15 publications

Supporting

Mentioning

223

Contrasting

Order By: Relevance

“…Several studies have shown that the induction of synaptic plasticity is accompanied by IE changes, indicating the involvement of concurrent changes in voltage-dependent ion channel activity in the soma membrane [1,9,53] . Activity-dependent regulation of IE induced by learning tasks has been reported in various animals [5,54,55] , and changes in the expression and/or gating kinetics of voltage-dependent ion channels in soma membranes influence IE after synaptic LTP (i.e., intrinsic plasticity) [5] .…”

Section: Modifi Cationsmentioning

confidence: 99%

“…This rapid and short-lasting reduction of I A via an inactivation curve shift during the initial period of potentiation can induce an initial and signifi cant enhancement of excitability throughout the neuron. In fact, activity-dependent changes in somatic I A channels are not unique because various conditioning stimuli for synaptic plasticity actively influence the expression and kinetic properties of several ion channels [1,53,[57][58][59][60] . Furthermore, it is possible that the I A -mediated enhancement of somatic excitability directly affects the properties and/or expression of other voltage-dependent ion channels, and thus modifi es membrane conductance and cellular signaling cascades (for review see Reyes 2001 [61] ).…”

Section: Modifi Cationsmentioning

confidence: 99%

“…The intrinsic excitability (IE) of neurons is defi ned as the ability to fi re APs with given certain synaptic inputs. Furthermore, in previous studies, the relationship between the summation of excitatory postsynaptic potentials (EPSPs) and AP firing has often been found to reflect the degree of IE [1][2][3][4][5] . In these studies, enhanced effi ciency of EPSP-AP coupling was demonstrated to be a typical property of neurons having high IE, which suggests a possible information-storage mechanism.…”

Section: Introductionmentioning

confidence: 99%

“…In these studies, enhanced effi ciency of EPSP-AP coupling was demonstrated to be a typical property of neurons having high IE, which suggests a possible information-storage mechanism. Although major cellular changes in synaptic plasticity are likely to be restricted to active synapses [6][7][8] , other studies have provided evidence that the induction of synaptic plasticity is accompanied by IE changes [1,9,10] . This correlation between synaptic plasticity and IE changes involves potential and concurrent changes in membrane factors, such as voltagegated ion channels, to regulate the membrane potential.…”

Section: Introductionmentioning

confidence: 99%

“…In mammalian hippocampal neurons, the total outward K + current can be simply divided into two types, a transient or rapidly inactivating current (A-type current, I A ), which is enhanced in dendrites, and a sustained or slow/non-inactivating current expressed at a constant somatodendritic density [1] . Genetic identification in Drosophila has revealed that several channel proteins encoded by the Shal family of K + channels (Kv4 channels) underlie the major I A in the somatodendritic compartment of neurons and show a more hyperpolarized voltage-dependence of gating properties [11,12] , while Shaker channels (Kv1) are localized exclusively to muscle cells [13] .…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Roles of somatic A-type K+ channels in the synaptic plasticity of hippocampal neurons

et al. 2014

View full text Add to dashboard Cite

In the mammalian brain, information encoding and storage have been explained by revealing the cellular and molecular mechanisms of synaptic plasticity at various levels in the central nervous system, including the hippocampus and the cerebral cortices. The modulatory mechanisms of synaptic excitability that are correlated with neuronal tasks are fundamental factors for synaptic plasticity, and they are dependent on intracellular Ca 2+ -mediated signaling. In the present review, the A-type K + (I A ) channel, one of the voltage-dependent cation channels, is considered as a key player in the modulation of Ca 2+ infl ux through synaptic NMDA receptors and their correlated signaling pathways. The cellular functions of I A channels indicate that they possibly play as integral parts of synaptic and somatic complexes, completing the initiation and stabilization of memory.

show abstract

Section: Modifi Cationsmentioning

confidence: 99%

Section: Modifi Cationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Roles of somatic A-type K+ channels in the synaptic plasticity of hippocampal neurons

et al. 2014

View full text Add to dashboard Cite

show abstract

Memory: Mechanisms Other than LTP

Debanne¹,

Campanac²

2009

Encyclopedia of Life Sciences

View full text Add to dashboard Cite

Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage. Long‐term changes in neuronal excitability have been reported in several brain areas following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Similarly to synaptic plasticity, long‐lasting intrinsic plasticity is bidirectional and expresses a certain level of input or cell specificity. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram. Key concepts: Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.

show abstract

Memory (Mechanisms Other than LTP )

Debanne

Campanac

2014

Encyclopedia of Life Sciences

View full text Add to dashboard Cite

Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage. Long‐term changes in neuronal excitability have been reported in several brain areas following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side, that is, in the axon, soma and dendrites of central neurons. Intrinsic plasticity is expressed in virtually all neuronal types including principal cells and interneurons. It is mediated by changes in the expression level or biophysical properties of voltage‐gated ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Similarly to synaptic plasticity, long‐lasting intrinsic plasticity is bidirectional and expresses a certain level of input or cell specificity. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram. Key Concepts: Synaptic plasticity is a major mode of memory storage. Persistent regulation of voltage‐gated ionic channels also participates in information storage following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of voltage‐gated ion channels in the membrane. Intrinsic plasticity can affect many different neuronal operations such as dendritic integration, action potential generation, action potential shape, action potential propagation and backpropagation. Synaptic and intrinsic plasticities share common learning rules and induction pathways. Synaptic and intrinsic plasticities contribute in synergy to the formation of a coherent mnesic engram.

show abstract

Rapid, synaptically driven increases in the intrinsic excitability of cerebellar deep nuclear neurons

Cited by 247 publications

References 15 publications

Roles of somatic A-type K+ channels in the synaptic plasticity of hippocampal neurons

Roles of somatic A-type K+ channels in the synaptic plasticity of hippocampal neurons

Memory: Mechanisms Other than LTP

Memory (Mechanisms Other than LTP )

Contact Info

Product

Resources

About