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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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Related Experiment Video

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Extrasynaptic NMDA Receptor in Excitotoxicity: Function Revisited.

Xianju Zhou1, Zhuoyou Chen1, Wenwei Yun1

  • 1Department of Neurology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, China.

The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry
|August 30, 2014
PubMed
Summary
This summary is machine-generated.

Proper N-methyl-D-aspartate receptor (NMDAR) activation aids brain function, while excessive activation causes neurodegeneration. New findings show cell death depends on co-activation of synaptic and extrasynaptic NMDARs, highlighting the need to revisit extrasynaptic NMDAR roles.

Keywords:
calciumexcitotoxicityextrasynaptic NMDARneurodegenerationsynaptic NMDAR

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Neuropharmacology

Background:

  • N-methyl-D-aspartate receptors (NMDARs) are crucial for neuronal survival and plasticity.
  • Dysregulated NMDAR activation contributes to neurodegeneration.
  • NMDARs exist at both synaptic and extrasynaptic locations, with distinct functional roles.

Purpose of the Study:

  • To investigate the differential roles of synaptic and extrasynaptic NMDARs in neuronal function and fate.
  • To explore how the co-activation of synaptic and extrasynaptic NMDARs influences neurodegeneration.
  • To inform the development of targeted therapeutic strategies for neurological disorders.

Main Methods:

  • Analysis of NMDAR function at synaptic and extrasynaptic sites.
  • Investigation of cellular responses to neuronal insults under varying NMDAR activation conditions.
  • Evaluation of the impact of synaptic versus extrasynaptic NMDAR co-activation on neuronal cell death.

Main Results:

  • Neuronal cell death following insults is dependent on the magnitude and duration of co-activation of both synaptic and extrasynaptic NMDARs.
  • Evidence suggests both synaptic and extrasynaptic NMDARs are involved in pathological processes.
  • Physiological brain functions also engage extrasynaptic NMDARs.

Conclusions:

  • The function of extrasynaptic NMDARs in cell fate requires re-evaluation.
  • Targeted antagonists for synaptic or extrasynaptic NMDARs could offer novel therapeutic avenues.
  • Understanding subcellular NMDAR localization is key to modulating neuronal survival and neuroplasticity.