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Related Concept Videos

Synaptic Signaling01:09

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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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Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
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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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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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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

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Presynaptically Silent Synapses Studied with Light Microscopy
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Shaping Neuronal Network Activity by Presynaptic Mechanisms.

Ayal Lavi1, Omri Perez2, Uri Ashery1

  • 1Department of Neurobiology, Life Sciences Institute, Tel Aviv University, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.

Plos Computational Biology
|September 16, 2015
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Summary
This summary is machine-generated.

This study introduces a new computational model for neuronal networks that simulates synaptic release mechanisms. The model explains how synaptic processes influence network activity, synchronization, and predicts correlations between vesicle dynamics and network bursts.

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Area of Science:

  • Computational Neuroscience
  • Systems Neuroscience
  • Neurobiology

Background:

  • Neuronal microcircuits exhibit oscillatory activity crucial for functions like sleep and learning.
  • Existing computational models often overlook direct simulation of synaptic transmission, limiting explanations for network activity changes.
  • Synaptic release mechanisms, including vesicle dynamics and calcium-dependent release, are key to neuronal interactions.

Purpose of the Study:

  • To develop a novel neuronal network model incorporating presynaptic release mechanisms.
  • To investigate how synaptic transmission parameters influence spontaneous neuronal network activity.
  • To provide mechanistic explanations for experimental findings in neuronal microcircuits.

Main Methods:

  • Developed a modified leaky integrate-and-fire neuron model.
  • Incorporated presynaptic release mechanisms: vesicle pool dynamics and calcium-dependent release probability.
  • Simulated spontaneous activity of neuronal networks and compared with experimental data.

Main Results:

  • The model generates spontaneous network activity patterns similar to experimental data.
  • Network activity remained robust despite changes in parameters like excitatory postsynaptic potential and connectivity.
  • The model explained network burst termination and effects of pharmacological/genetic manipulations.
  • Elevated asynchronous release, not spontaneous release, was shown to synchronize network activity.
  • Asynchronous release enhances recycling vesicle pool utilization for network effects.
  • Predicted and experimentally supported a positive correlation between vesicle priming and network burst frequency.

Conclusions:

  • Synaptic release processes at the neuronal level significantly govern activity patterns and synchronization at the network level.
  • The model provides a mechanistic framework for understanding how synaptic transmission shapes network dynamics.
  • This approach offers insights into the functional consequences of synaptic vesicle dynamics in neuronal circuits.