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Excitatory and Inhibitory Effects of Neurotransmitters01:29

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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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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 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
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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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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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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.
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Modification of the synaptic cleft under excitatory conditions.

Jung-Hwa Tao-Cheng1, Sandra L Moreira1, Christine A Winters2

  • 1NINDS Electron Microscopy Facility, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD, United States.

Frontiers in Synaptic Neuroscience
|October 16, 2023
PubMed
Summary

Excitatory conditions widen the synaptic cleft, creating "open clefts" by dissociating calcium-dependent bridges. This structural change may facilitate neurotransmitter clearance and receptor mobility, potentially serving a homeostatic function.

Keywords:
electron microscopyexcitatorysynaptic activitysynaptic clefttranssynaptic bridge

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Synaptic Plasticity

Background:

  • The synaptic cleft, crucial for neuronal communication, is increasingly recognized for its role in synaptic efficacy.
  • Its precise geometry and molecular organization significantly influence synaptic function.

Purpose of the Study:

  • To investigate short-term morphological changes in the synaptic cleft under excitatory conditions using electron microscopy.
  • To understand how synaptic cleft structure is affected by neuronal activity and chemical modulators.

Main Methods:

  • Utilized electron microscopy to examine synaptic structures in cultured hippocampal neurons and adult brain tissue.
  • Applied high potassium (K+) concentrations, tetrodotoxin (TTX), NMDA, APV, and EGTA to manipulate neuronal activity and calcium levels.

Main Results:

  • High K+ depolarization and NMDA application significantly increased the frequency of peripherally widened synaptic clefts ('open clefts').
  • TTX application, inhibiting basal activity, led to the disappearance of open clefts.
  • Extracellular calcium depletion using EGTA also increased open cleft frequency, suggesting the role of Ca2+-dependent trans-synaptic bridges.

Conclusions:

  • Excitatory conditions and calcium depletion promote synaptic cleft widening, likely by dissociating trans-synaptic bridges.
  • This structural plasticity may allow mobile elements like AMPA receptors into the cleft.
  • Peripheral cleft opening could enhance neurotransmitter clearance, potentially acting as a homeostatic or protective mechanism.