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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.
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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.
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Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
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Myosin IXa Binds AMPAR and Regulates Synaptic Structure, LTP, and Cognitive Function.

Alessandra Folci1, Luca Murru2, Elena Vezzoli3

  • 1CNR Institute of NeuroscienceMilano, Italy; Institute of Biophysics, Medical University of GrazGraz, Austria.

Frontiers in Molecular Neuroscience
|February 3, 2016
PubMed
Summary

Myosin IXa (Myo9a) is crucial for hippocampal synapse structure and function. Its absence impairs synaptic transmission, long-term potentiation, and cognitive abilities in mice.

Keywords:
AMPARLTPMyosin IXaPSDhippocampal synapses

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Myosin IXa (Myo9a) is a brain-abundant motor protein.
  • Its specific role in neuronal function is currently unknown.

Purpose of the Study:

  • To investigate the function of Myosin IXa (Myo9a) in hippocampal synapses.
  • To elucidate Myo9a's role in synaptic structure and plasticity.

Main Methods:

  • Localization studies of Myo9a in rat hippocampal neurons.
  • Co-immunoprecipitation to identify Myo9a binding partners.
  • Analysis of synaptic structure, protein expression, and synaptic function in Myo9a(+/-) mice.
  • Assessment of long-term potentiation (LTP) and cognitive functions.

Main Results:

  • Myo9a localizes to the postsynaptic density (PSD) and binds the AMPAR GluA2 subunit.
  • Myo9a deficiency leads to a thicker PSD, increased PSD95, and elevated surface AMPAR expression.
  • Synaptic transmission, LTP, and cognitive functions are impaired in Myo9a(+/-) mice.

Conclusions:

  • Myosin IXa (Myo9a) plays a critical role in regulating the molecular architecture of hippocampal synapses.
  • Myo9a is essential for maintaining normal synaptic transmission, plasticity, and cognitive function.