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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.
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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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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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...
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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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The Synapse02:47

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Neurons communicate with one another by passing on their electrical signals to other neurons. A synapse is the location where two neurons meet to exchange signals. At the synapse, the neuron that sends the signal is called the presynaptic cell, while the neuron that receives the message is called the postsynaptic cell. Note that most neurons can be both presynaptic and postsynaptic, as they both transmit and receive information.
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Synaptic Signaling01:09

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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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Shank Proteins Differentially Regulate Synaptic Transmission.

Rebecca Shi1,2,3, Patrick Redman1, Dipanwita Ghose1

  • 1Picower Institute for Learning and Memory, Cambridge, MA 02139.

Eneuro
|December 19, 2017
PubMed
Summary
This summary is machine-generated.

Shank proteins regulate glutamatergic synaptic transmission. Loss of Shank1 or Shank2 reduces AMPAR synapse numbers, while combined loss and NMDAR deficits occur with Shank1/Shank2 knockdown, requiring intact SAM domains for function.

Keywords:
ASDProsap1bicucullineexcitatoryhippocampusmini

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Shank proteins are key scaffolds in the postsynaptic density (PSD) of glutamatergic synapses.
  • Dysfunction of Shank proteins is linked to autism spectrum disorders and neuropsychiatric diseases.
  • Distinct roles of Shank family members in synaptic transmission regulation remain unclear.

Purpose of the Study:

  • Investigate the specific functions of Shank proteins in regulating glutamatergic synaptic transmission.
  • Compare the roles of different Shank proteins and their differences from other scaffold proteins.
  • Determine the necessity of the sterile alpha motif (SAM) domain for Shank protein function.

Main Methods:

  • Lentivirus-mediated knockdown of Shank proteins in rat hippocampal slice cultures.
  • Molecular replacement strategies to restore Shank protein function.
  • Dual whole-cell patch clamp recordings to assess synaptic transmission.
  • Analysis of AMPA and NMDA receptor-mediated synaptic responses.

Main Results:

  • Knockdown of Shank1 or Shank2, but not Shank3, reduced AMPAR-containing synapse numbers without altering unitary responses.
  • Combined Shank1 and Shank2 knockdown decreased both synapse number and unitary response, alongside reduced NMDAR function.
  • Molecular replacement with Shank2 and Shank3c restored synaptic transmission; intact SAM domains were essential.
  • Shank1/Shank2 knockdown effects on AMPAR transmission were independent of altered neural activity, unlike PSD-95 knockdown.

Conclusions:

  • Shank1 and Shank2 play distinct, partially overlapping roles in maintaining glutamatergic synapse structure and function.
  • The sterile alpha motif (SAM) domain is critical for Shank proteins' role in synaptic transmission.
  • Shank proteins interact differently with activity-dependent signaling pathways compared to other scaffolds like PSD-95.