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Related Concept Videos

Overview of Synapses01:25

Overview of Synapses

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A synapse is a specialized structure where two neurons connect, allowing them to pass an electrical or chemical signal to another neuron. It is the point of communication between neurons. The term "synapse" is derived from the Greek word "synapsis," which means "conjunction." The entire process of neural communication revolves around the synapse. When activated, a neuron releases chemicals known as neurotransmitters into the synapse. These neurotransmitters cross the synapse and bind to...
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Integration of Synaptic Events01:28

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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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Fusion of Secretory Vesicles with the Plasma Membrane01:26

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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
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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.
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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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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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Identification and Classification of Position-specific GABAA Receptor Subunit Missense Variants for Their Role In Hippocampal Pyramidal Neurons
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Synapsin Isoforms Regulating GABA Release from Hippocampal Interneurons.

Sang-Ho Song1, George J Augustine2

  • 1Center for Functional Connectomics, Korea Institute of Science and Technology, Seoul, Republic of Korea 136-791, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 138673, Singapore, and Institute of Molecular and Cell Biology, Singapore 138673, Singapore.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|June 24, 2016
PubMed
Summary

Synapsins regulate GABA release, with multiple isoforms supporting release and synchrony in hippocampal interneurons. This differs from glutamatergic terminals, highlighting distinct synapsin roles in neurotransmission.

Keywords:
GABAexocytosishippocampusinterneuronssynapsinsynaptic vesicle trafficking

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Synapsins are crucial for synaptic vesicle (SV) trafficking.
  • The specific synapsin isoforms regulating GABA release remain largely unknown.
  • Understanding neurotransmitter release is vital for brain function.

Purpose of the Study:

  • Identify synapsin isoforms regulating GABA release in hippocampal interneurons.
  • Investigate the distinct roles of synapsins in GABAergic versus glutamatergic neurotransmission.
  • Elucidate synapsin function in SV release kinetics and synchrony.

Main Methods:

  • Utilized synapsin I, II, and III triple knock-out (TKO) mice.
  • Performed rescue experiments with cultured hippocampal neurons.
  • Employed in situ hybridization to detect synapsin isoform expression.
  • Analyzed evoked inhibitory postsynaptic currents (IPSCs) and release kinetics using deconvolution.

Main Results:

  • Five synapsin isoforms are expressed in hippocampal interneurons, all rescuing evoked IPSC amplitude in TKO neurons.
  • Unlike glutamatergic terminals, multiple synapsin isoforms rescue the TKO phenotype for GABA release.
  • Synapsins, except synapsin IIIa, rescue impaired GABA release kinetics in TKO neurons.
  • Synapsins regulate GABA release from the readily releasable pool and control release synchrony.

Conclusions:

  • Synapsins play diverse roles in regulating GABA release compared to other neurotransmitters.
  • Multiple synapsin isoforms contribute to GABA release and synchrony in hippocampal interneurons.
  • Synapsins exhibit fundamentally distinct functions at different presynaptic terminal types.