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Chemical Synapses

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.
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 Synapses

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.
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...

Long-term Potentiation

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 Potentiation

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.

Ligand-Gated Ion Channel Receptor: Gating Mechanism

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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

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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Related Experiment Video

Updated: Jun 1, 2026

Presynaptically Silent Synapses Studied with Light Microscopy

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

Homeostatic synaptic plasticity through changes in presynaptic calcium influx.

CongJian Zhao¹, Elena Dreosti, Leon Lagnado

¹Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 0QH, United Kingdom.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|May 20, 2011

Summary

Network activity changes synaptic strength through presynaptic mechanisms. Reduced activity increases calcium influx and vesicle fusion, driven by presynaptic calcium channels, impacting neural circuit homeostasis.

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Presynaptically Silent Synapses Studied with Light Microscopy

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Published on: January 4, 2010

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Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Published on: March 15, 2018

Area of Science:

Neuroscience
Synaptic Plasticity
Neural Circuits

Background:

Homeostatic synaptic plasticity compensates for chronic neural network perturbations.
Postsynaptic mechanisms are understood, but presynaptic mechanisms altering neurotransmitter release efficiency remain unclear.

Purpose of the Study:

To investigate the role of presynaptic calcium influx in homeostatic synaptic plasticity.
To elucidate the presynaptic mechanisms underlying compensatory changes in synaptic strength.

Main Methods:

Utilized cultured hippocampal neurons.
Employed two fluorescent proteins: SyGCaMP2 (synaptic vesicle calcium reporter) and SypHy (vesicle fusion reporter).

Main Results:

Decreased network activity led to increased presynaptic calcium influx per action potential.
Reduced network activity resulted in a higher probability of vesicle fusion.
Homeostatic changes in release probability showed a cubic relationship with calcium influx.

Conclusions:

Presynaptic calcium channels are key determinants of homeostatic synaptic strength changes.
Modifications in the number or function of presynaptic calcium channels significantly impact synaptic plasticity.