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Related Concept Videos

Chemical Synapses01:26

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.
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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.
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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.
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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.
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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...
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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

Updated: Apr 14, 2026

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
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Homeostatic synaptic depression is achieved through a regulated decrease in presynaptic calcium channel abundance.

Michael A Gaviño1, Kevin J Ford1, Santiago Archila1

  • 1Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, United States.

Elife
|April 18, 2015
PubMed
Summary
This summary is machine-generated.

This study reveals how synaptic transmission is bidirectionally controlled at the neuromuscular junction. Homeostatic depression, a key process, is achieved by reducing presynaptic calcium channels, independent of action potentials.

Keywords:
CaV2.1D. melanogasterbrainhomeostatic plasticityneuromuscular junctionneuroscienceneurotransmissionsynapse

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • Homeostatic signaling stabilizes synaptic transmission at the neuromuscular junction (NMJ).
  • Mechanisms for homeostatic potentiation of neurotransmitter release are known, but homeostatic depression is poorly understood.
  • Bi-directional plasticity at the NMJ is crucial for stable neural function.

Purpose of the Study:

  • To elucidate the mechanisms underlying homeostatic depression at the NMJ.
  • To investigate how bi-directional synaptic plasticity is achieved.
  • To determine if potentiation and depression are genetically separable processes.

Main Methods:

  • Inducing simultaneous homeostatic potentiation and depression.
  • Utilizing genetic mutations to block homeostatic potentiation.
  • Measuring presynaptic calcium channel abundance and calcium influx.
  • Assessing changes independent of the presynaptic action potential waveform.

Main Results:

  • Demonstrated that homeostatic potentiation and depression can occur simultaneously, proving true bi-directional plasticity.
  • Showed that mutations affecting potentiation do not impact depression, indicating genetic separability.
  • Identified decreased presynaptic calcium channel abundance and influx as the mechanism for homeostatic depression.
  • Confirmed that these depression mechanisms are independent of action potential waveform.

Conclusions:

  • Identified a novel mechanism for homeostatic synaptic plasticity.
  • Proposed a model explaining bi-directional, homeostatic control of presynaptic neurotransmitter release.
  • Highlighted the distinct genetic pathways governing synaptic potentiation and depression.