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Neuroplasticity01:01

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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.
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.
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Long-term Potentiation01:35

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Related Experiment Video

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Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
12:47

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Published on: March 20, 2014

Astrocyte-mediated distributed plasticity at hypothalamic glutamate synapses.

Grant R J Gordon1, Karl J Iremonger, Srinivas Kantevari

  • 1Hotchkiss Brain Institute, Department of Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada.

Neuron
|November 17, 2009
PubMed
Summary

Astrocytes mediate rapid, distributed synaptic plasticity by releasing ATP in response to neural activity. This astrocyte-driven mechanism enhances glutamate synapse strength, scaling synaptic efficacy across the neuron.

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Area of Science:

  • Neuroscience
  • Cellular Neuroscience
  • Synaptic Plasticity

Background:

  • Synaptic efficacy can be rapidly modulated by afferent activity.
  • Synaptic plasticity mechanisms are crucial for neural computation and memory.

Purpose of the Study:

  • To investigate a novel form of synaptic plasticity involving astrocyte recruitment.
  • To elucidate the mechanisms underlying fast, feed-forward synaptic scaling mediated by astrocytes.

Main Methods:

  • Combined electrophysiology, caged molecule photolysis, and calcium imaging.
  • Investigated synaptic currents at glutamate synapses on magnocellular neurosecretory cells.
  • Examined the role of astrocytes and gliotransmitters in synaptic plasticity.

Main Results:

  • Afferent activity recruits astrocytes, leading to a fast, feed-forward increase in quantal synaptic current amplitude.
  • This plasticity results in a multiplicative scaling of synaptic strength across multiple synapses.
  • Astrocyte activation requires metabotropic glutamate receptor-mediated calcium rise and ATP release, acting on postsynaptic purinergic receptors.

Conclusions:

  • Astrocytes mediate a novel form of distributed synaptic plasticity.
  • This plasticity is fast, feed-forward, and triggered by synaptic activity.
  • Gliotransmitter release from astrocytes, specifically ATP, is essential for synaptic scaling.