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Related Concept Videos

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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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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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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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 PSD-95 biology: from localization and interactors to N-terminus function.

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This review explores how the postsynaptic density protein-95 (PSD-95) regulates synaptic plasticity, specifically long-term depression (LTD). It details how modifications to PSD-95 control its membrane association, influencing learning and memory.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), is crucial for learning and memory.
  • The postsynaptic density protein-95 (PSD-95) plays a key role in organizing the postsynaptic density (PSD) and synaptic signaling pathways.
  • N-methyl-D-aspartate receptor (NMDAR)-dependent LTD is a critical form of synaptic plasticity.

Purpose of the Study:

  • To examine the role of PSD-95 in synaptic plasticity, focusing on NMDAR-dependent LTD.
  • To elucidate how posttranslational modifications (PTMs) of PSD-95 influence its function in synaptic plasticity.
  • To present a model integrating nanoscale crowding, PTM gating, and protein interactions in LTD initiation and maintenance.

Main Methods:

  • Review of existing literature on PSD-95, synaptic plasticity, and NMDAR-dependent LTD.
  • Emphasis on posttranslational modifications (PTMs) of the N-terminal domain of PSD-95.
  • Synthesis of evidence regarding phosphorylation-dependent cis-trans isomerization regulating palmitoylation and membrane association.

Main Results:

  • PSD-95's N-terminal domain PTMs critically affect its synaptic localization and stability.
  • Phosphorylation-dependent cis-trans isomerization regulates PSD-95 palmitoylation and membrane association.
  • A model is proposed where nanoscale crowding, PTM gating, and modular interactions govern LTD at excitatory synapses.

Conclusions:

  • PSD-95 is a central regulator of synaptic plasticity, particularly NMDAR-dependent LTD.
  • PTMs of PSD-95, including phosphorylation and palmitoylation, are key mechanisms controlling its synaptic function.
  • The proposed model provides a framework for understanding the local initiation and maintenance of LTD at the molecular level.