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Long-term Potentiation01:35

Long-term Potentiation

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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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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...
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Long-term Depression01:03

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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Desensitization and Tachyphylaxis01:20

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Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
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Excitatory and Inhibitory Effects of Neurotransmitters01:29

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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...
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Related Experiment Video

Updated: Jun 28, 2025

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System
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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

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Enhanced Release Probability without Changes in Synaptic Delay during Analogue-Digital Facilitation.

Sami Boudkkazi1,2, Dominique Debanne2

  • 1Physiology Institute, University of Freiburg, 79104 Freiburg, Germany.

Cells
|April 12, 2024
PubMed
Summary
This summary is machine-generated.

Synaptic delay remains unchanged during depolarization-induced analogue-digital facilitation (d-ADF) despite increased presynaptic release probability. This indicates compensatory mechanisms involving action potential changes maintain precise neuronal timing.

Keywords:
context-dependent facilitationlocal circuitsneocortexneuronal timingsynaptic latencysynaptic transmission

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Computational Neuroscience

Background:

  • Neuronal timing is crucial for brain functions like perception and memory.
  • Synaptic delay is influenced by presynaptic release probability and action potential waveform.
  • Existing research links synaptic delay changes to various forms of synaptic plasticity.

Purpose of the Study:

  • To investigate whether synaptic delay is modulated during depolarization-induced analogue-digital facilitation (d-ADF).
  • To understand the interplay between release probability and action potential dynamics in synaptic delay during d-ADF.

Main Methods:

  • Electrophysiological recordings from pyramidal L5-L5 cell synapses.
  • Induction of d-ADF through prolonged presynaptic depolarization.
  • Analysis of synaptic delay, release probability, and action potential properties.

Main Results:

  • Depolarization-induced analogue-digital facilitation (d-ADF) elevated presynaptic release probability (Pr).
  • Despite elevated Pr, synaptic delay at L5-L5 cell synapses remained unchanged during d-ADF.
  • Voltage-inactivation of presynaptic Kv1 channels mediated d-ADF.

Conclusions:

  • Synaptic timing is unaffected during d-ADF due to compensatory interactions.
  • Presynaptic release probability and action potential-dependent modulations of synaptic delay balance each other.
  • Unlike other plasticity forms, d-ADF preserves synaptic timing precision.