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Related Concept Videos

The Role of Ion Channels in Neuronal Computation01:19

The Role of Ion Channels in Neuronal Computation

A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
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Long-term Potentiation01:35

Long-term Potentiation

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Graded Potential01:19

Graded Potential

Graded potentials are localized fluctuations in the cell membrane's electrical charge, commonly found in the dendrites of neurons. The magnitude of these potential changes depends on the strength of the initiating stimulus. In a membrane at its resting potential, a graded potential signifies a voltage shift either above -70 mV or below -70 mV.
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Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

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Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus
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Pyramidal neuron conductance state gates spike-timing-dependent plasticity.

Jary Y Delgado1, José F Gómez-González, Niraj S Desai

  • 1The Neurosciences Institute, San Diego, CA 92121, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|November 26, 2010
PubMed
Summary

Ongoing synaptic background activity selectively reduces spike-timing dependent plasticity (STDP) potentiation in neocortical neurons. This effect sharpens STDP curves and may act as a homeostatic mechanism against runaway synaptic potentiation.

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Area of Science:

  • Neuroscience
  • Computational Neuroscience
  • Synaptic Plasticity

Background:

  • Neocortical neurons integrate inputs amidst significant background synaptic activity.
  • The impact of background activity on spike-timing dependent plasticity (STDP) remains unclear.
  • Understanding synaptic plasticity is crucial for comprehending neural network function.

Purpose of the Study:

  • To investigate the effect of simulated synaptic background activity on STDP in rat neocortical pyramidal cells.
  • To determine whether background activity differentially affects synaptic potentiation and depression.
  • To elucidate the underlying mechanisms of conductance-dependent regulation of synaptic plasticity.

Main Methods:

  • Dynamic-clamp system to inject simulated background conductances into pyramidal cells.
  • Dual somatic and dendritic patch-clamp recordings in rat brain slices.
  • Biophysically detailed computational modeling of neuronal activity and plasticity.

Main Results:

  • Simulated background conductances selectively reduced the magnitude of timing-dependent synaptic potentiation.
  • Synaptic depression magnitude remained unchanged under background activity.
  • Background activity sharpened the STDP curve, requiring tighter temporal pairing for potentiation.
  • Shunting of dendritic excitatory postsynaptic potentials (EPSPs) and action potentials (APs) was identified as a key mechanism.
  • Computational models revealed truncation of dendritic spine calcium dynamics affecting potentiation more than depression.

Conclusions:

  • Synaptic background activity exerts a selective suppressive effect on spike-timing dependent plasticity potentiation.
  • This suppression may serve as a homeostatic mechanism to prevent excessive Hebbian network potentiation.
  • The findings highlight a novel form of conductance-dependent regulation of synaptic plasticity.