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Chemical Synapses01:26

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 Synapses01:26

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...

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Related Experiment Video

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Short-term synaptic plasticity is altered in mice lacking synapsin I

T W Rosahl1, M Geppert, D Spillane

  • 1Department of Molecular Genetics, Howard Hughes Medical Institute, University of Texas Southwestern Medical School, Dallas 75235.

Cell
|November 19, 1993
PubMed
Summary

Synapsin I is not essential for neurotransmitter release, as mice lacking this protein show no major functional deficits. However, its absence selectively increases paired pulse facilitation, suggesting a role in regulating release.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Synapsin I is a key phosphoprotein in synaptic vesicles, believed to be crucial for neurotransmitter release.
  • Its precise role in regulating synaptic transmission remains incompletely understood.

Purpose of the Study:

  • To investigate the necessity of synapsin I for neurotransmitter release by creating a null mutation in the synapsin I gene.
  • To characterize the functional consequences of synapsin I deficiency in mice.

Main Methods:

  • Homologous recombination was used to generate synapsin I-deficient (null mutation) mice.
  • Electrophysiological recordings were performed to assess synaptic transmission parameters.

Main Results:

  • Mice lacking synapsin I exhibited no observable deficits in overall well-being or gross nervous system function.
  • Electrophysiology revealed a selective increase in paired pulse facilitation in synapsin I-null mice.
  • No significant alterations were observed in other synaptic parameters, including long-term potentiation.

Conclusions:

  • Synapsin I is not essential for the fundamental process of neurotransmitter release.
  • Synapsin I may play a role in limiting excessive neurotransmitter release by modulating residual calcium levels after stimulation.
  • Redundant mechanisms likely compensate for the loss of synapsin I function in basic neurotransmission.