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Related Concept Videos

Long-term Depression01:05

Long-term Depression

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.
Long-term Depression01:03

Long-term Depression

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.
Calcium Ion Concentration Mechanism
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Long-term Potentiation01:35

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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.
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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Chemical Synapses01:26

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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.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

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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Related Experiment Video

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Paired Whole Cell Recordings in Organotypic Hippocampal Slices
09:23

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Release-dependent variations in synaptic latency: a putative code for short- and long-term synaptic dynamics.

Sami Boudkkazi1, Edmond Carlier, Norbert Ankri

  • 1INSERM U641, Marseille, F-13916 France.

Neuron
|December 21, 2007
PubMed
Summary
This summary is machine-generated.

Synaptic latency in the cortex, typically ignored, is actually linked to presynaptic release probability (Pr). This finding reveals a new way neurons communicate, impacting synaptic plasticity and network dynamics.

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Area of Science:

  • Neuroscience
  • Computational Neuroscience

Background:

  • Synaptic latencies in cortical circuits are typically considered negligible, with variations around 1-2 ms.
  • The functional significance of these small latency variations remains largely unexplored.

Purpose of the Study:

  • To investigate the relationship between synaptic latency and presynaptic release probability (Pr) in cortical neurons.
  • To determine if synaptic latency variations play a role in short- and long-term synaptic plasticity.

Main Methods:

  • Electrophysiology in monosynaptically connected L5 and CA3 pyramidal neurons.
  • Manipulation of presynaptic release probability (Pr).
  • Dynamic-clamp technique to assess the impact of latency-strength covariation.

Main Results:

  • Synaptic latency is inversely correlated with postsynaptic current amplitude and directly influenced by Pr.
  • Paired-pulse depression and facilitation were associated with increased and decreased synaptic latencies, respectively.
  • Long-term depression (LTD) prolonged latency, while long-term potentiation (LTP) reduced it, demonstrating latency changes with plasticity.

Conclusions:

  • Amplitude-related variations in synaptic latency are not negligible and are modulated by Pr.
  • These latency dynamics are integral to short- and long-term synaptic plasticity.
  • The covariation of synaptic latency and strength significantly impacts postsynaptic spiking and cortical network function.