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Related Concept Videos

Integration of Synaptic Events01:28

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...
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
LTP can occur when presynaptic neurons...
Long-term Potentiation01:35

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.
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
Synaptic Signaling01:09

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
Synaptic Signaling01:12

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.

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Related Experiment Video

Updated: Jun 13, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons
11:48

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Published on: July 13, 2011

Synaptic activity controls dendritic spine morphology by modulating eEF2-dependent BDNF synthesis.

Chiara Verpelli1, Giovanni Piccoli, Cristina Zibetti

  • 1Consiglio Nazionale delle Ricerche Neuroscience Institute, Milan, Italy.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|April 30, 2010
PubMed
Summary

The eukaryotic elongation factor 2 kinase (eEF2K) pathway controls neuronal plasticity by regulating the synthesis of brain-derived neurotrophic factor (BDNF) in dendrites, essential for learning and memory.

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Last Updated: Jun 13, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons
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Published on: July 13, 2011

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Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Synaptic plasticity, crucial for learning and memory, relies on activity-dependent protein translation.
  • Dendritic spine morphology and stability are key determinants of synaptic function.

Purpose of the Study:

  • To investigate the role of eukaryotic elongation factor 2 kinase (eEF2K) in regulating synaptic structure and function.
  • To elucidate the mechanism by which eEF2K influences dendritic BDNF synthesis and spine plasticity.

Main Methods:

  • RNAi knockdown and overexpression of eEF2K in neurons.
  • Analysis of dendritic spine stability and morphology.
  • Measurement of BDNF protein expression in dendrites.
  • Investigation of mGluR/eEF2K signaling pathways.

Main Results:

  • eEF2K knockdown decreased dendritic spine stability and BDNF expression.
  • eEF2K overexpression promoted spine maturation and increased BDNF levels.
  • BDNF overexpression rescued spine stability defects caused by eEF2K knockdown.
  • Synaptic activity-induced spine maturation and BDNF expression depend on mGluR/eEF2K signaling.

Conclusions:

  • The eEF2K/eEF2 pathway acts as a critical sensor coupling neuronal activity to spine plasticity.
  • eEF2K regulates dendritic BDNF translation, thereby controlling synaptic structure and function.
  • This pathway is essential for the molecular mechanisms underlying learning and memory.