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Related Concept Videos

Excitatory and Inhibitory Effects of Neurotransmitters01:29

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 specific...
Chemical Synapses01:26

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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...
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Ligand-Gated Ion Channel Receptor: Gating Mechanism

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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Neurochemical Transmission: Sites of Drug Action

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...
Chemical Synapses01:26

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Postsynaptic Potential (PSP)

Postsynaptic potential (PSP) refers to a change in the electrical potential of a neuron when neurotransmitters released by presynaptic neurons bind to postsynaptic receptors. This potential can either be excitatory, leading to depolarization and ultimately action potential generation, or inhibitory, leading to hyperpolarization and suppression of the postsynaptic neuron.
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Updated: Jul 19, 2026

Dopamine Release at Individual Presynaptic Terminals Visualized with FFNs
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Published on: August 31, 2009

Proton release as a modulator of presynaptic function.

S F Traynelis1, M Chesler

  • 1Department of Pharmacology, Emory University School of Medicine, Rollins Research Center, 1510 Clifton Road, Atlanta, GA 30322, USA.

Neuron
|January 5, 2002
PubMed
Summary

Acidification of the synaptic cleft may reduce calcium channel activity, acting as a brake on glutamate release from cone cells. This finding suggests a novel mechanism for regulating synaptic transmission.

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Published on: August 16, 2018

Area of Science:

  • Neuroscience
  • Synaptic Physiology
  • Cellular Signaling

Background:

  • Synaptic transmission relies on the release of neurotransmitters like glutamate.
  • Calcium ions (Ca2+) play a crucial role in neurotransmitter release.
  • Cone cells are photoreceptor cells in the retina responsible for color vision.

Discussion:

  • DeVries (2001) investigated the role of synaptic cleft pH in regulating glutamate release.
  • Experiments suggest that a decrease in pH (acidification) can inhibit Ca2+ channel activity.
  • This inhibition of Ca2+ channels acts as a brake on the continuous (tonic) release of glutamate.

Key Insights:

  • Synaptic cleft acidification is a potential regulator of neurotransmitter release.
  • Reduced Ca2+ channel activity due to acidification limits glutamate release from cone cells.
  • This mechanism provides a new perspective on the control of synaptic signaling.

Outlook:

  • Further research is needed to elucidate the precise molecular mechanisms involved.
  • Understanding this regulatory pathway could have implications for retinal function and disease.
  • This discovery opens new avenues for exploring synaptic transmission modulation.