Homeostatic Regulation of Glutamate Release in Response to Depolarization
Abstract
Proper nervous system function requires a balance between excitation and inhibition. Systems of homeostasis may have evolved in neurons to help maintain or restore balance between excitation and inhibition, presumably because excessive excitation can cause dysfunction and cell death. This article reviews evidence for homeostatic mechanisms within the hippocampus that lead to differential regulation of glutamate and gamma-aminobutyric acid release in response to conditions of excess depolarization. We recently found differential effects on glutamate release at the level of action potential coupling to transmitter release, vesicular release probability, and vesicle availability. Such differential regulation may help to prevent excitotoxicity and runaway excitation.
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The decrease in the sensitivity of NMDA receptors during phase 2 would reduce calcium influx, thereby protecting hippocampal neurons from developing excitotoxicity in times of strong and persistent stress.
“The decrease in the sensitivity of NMDA receptors during phase 2 would reduce calcium influx, thereby protecting hippocampal neurons from developing excitotoxicity in times of strong and persistent stress (Moudy et al. [301]; Moulder et al. [302]).”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Moulder et al. [302]
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“However, these results are not universally accepted, and others have reported that BDNF can depress electrically evoked IPSCs (56).”
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Postsynaptic expression of homeostatic plasticity at neocortical synapses
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Postsynaptic Depolarization Scales Quantal Amplitude in Cortical Pyramidal Neurons
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Diamond, D. M., Campbell, A. M., Park, C. R., Halonen, J., & Zoladz, P. R. (2007) · Neural Plasticity · doi:10.1155/2007/60803 · Cited by 762 · see citing works
“The decrease in the sensitivity of NMDA receptors during phase 2 would reduce calcium influx, thereby protecting hippocampal neurons from developing excitotoxicity in times of strong and persistent stress (Moudy et al. [301]; Moulder et al. [302]).”
BackgroundUnraveling mechanisms of homeostatic synaptic plasticity
Pozo, K., & Goda, Y. (2010) · Neuron · doi:10.1016/j.neuron.2010.04.028 · Cited by 565 · see citing works
- Authors
- Moulder, K. L., Meeks, J. P., & Mennerick, S.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Mennerick, Steven
- Venue
- Molecular Neurobiology
- Published
- 2006
- Volume
- 33
- Issue
- 2
- Pages
- 133-154
- ISSN
- 0893-7648 (ISSN-L)
- OpenAlex
- W2004248029
- Cited by
- 26
- References
- 7
- Citations by year
- 2025: 1 · 2022: 1 · 2020: 1 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 1
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- homeostatic regulation, glutamate release, gamma-aminobutyric acid release, depolarization, excitation-inhibition balance, hippocampus, excitotoxicity
- MeSH terms
- Action Potentials, Animals, gamma-Aminobutyric Acid, Hippocampus, Homeostasis, Humans, Ion Channels, Neural Inhibition, Synaptic Transmission, Synaptic Vesicles, Presynaptic Terminals, Glutamic Acid
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