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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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Integration of Synaptic Events
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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 Depression
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Calcium Ion Concentration Mechanism
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Calcium Ion Concentration Mechanism
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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.
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...
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...
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Desensitization and Tachyphylaxis
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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
Summary
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 transmissionMore Related Videos
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.


