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Synaptic Signaling

Synaptic Signaling

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.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...

Synaptic Signaling

Synaptic Signaling

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.

Long-term Depression

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
If over...

Long-term Depression

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.

Excitatory and Inhibitory Effects of Neurotransmitters

Excitatory and Inhibitory Effects of Neurotransmitters

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...

Integration of Synaptic Events

Integration of Synaptic Events

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: Apr 29, 2026

A Method for Remotely Silencing Neural Activity in Rodents During Discrete Phases of Learning

A Method for Remotely Silencing Neural Activity in Rodents During Discrete Phases of Learning

Published on: June 22, 2015

Silencing synapses with DREADDs.

Hu Zhu¹, Bryan L Roth¹

¹Department of Pharmacology, 4072 Genetic Medicine Building, UNC Chapel Hill Medical School, Chapel Hill, NC 27514, USA.

|May 24, 2014

Summary

This summary is machine-generated.

Chemogenetic silencer hM4Di-DREADD inhibits presynaptic glutamate release. An axon-targeted variant allows localized silencing of synaptic transmission in neural circuits.

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Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Chemogenetics offers tools to modulate neuronal activity.
DREADDs (Designer Receptors Exclusively Activated by Designer Drugs) are widely used.
Presynaptic function is critical for neural communication.

Purpose of the Study:

To investigate the effect of hM4Di-DREADD on presynaptic glutamate release.
To develop and validate an axon-targeted hM4Di variant.
To assess the utility of this variant for localized circuit silencing.

Main Methods:

Utilized chemogenetics with hM4Di-DREADD.
Generated an axon-targeted hM4Di variant.
Measured presynaptic glutamate release.
Assessed synaptic transmission in neural circuits.

Main Results:

hM4Di-DREADD effectively suppresses presynaptic glutamate release.
The axon-targeted hM4Di variant specifically silences synaptic transmission.
Localized silencing of neural circuits is achievable.

Conclusions:

hM4Di-DREADD is a potent inhibitor of presynaptic glutamate release.
Axon-targeted hM4Di provides a tool for precise control of synaptic activity.
This technology enables targeted manipulation of neural circuit function.