Biology:Homeostatic plasticity
In neuroscience, homeostatic plasticity refers to the capacity of neurons to regulate their own excitability relative to network activity.[1][2] The term homeostatic plasticity derives from two opposing concepts: 'homeostatic' (a product of the Greek words for 'same' and 'state' or 'condition') and plasticity (or 'change'), thus homeostatic plasticity means "staying the same through change".
Comparison with Hebbian plasticity
Homeostatic synaptic plasticity is a means of maintaining the synaptic basis for learning, respiration, and locomotion, in contrast to the Hebbian plasticity associated with learning and memory.[3] Although Hebbian forms of plasticity, such as long-term potentiation and long-term depression occur rapidly, homeostatic plasticity (which relies on protein synthesis) can take hours or days.[4] TNF-α[5] and microRNAs[4] are important mediators of homeostatic synaptic plasticity.
Homeostatic plasticity is thought to balance Hebbian plasticity by modulating the activity of the synapse or the properties of ion channels. Homeostatic plasticity in neocortical circuits has been studied in depth by Gina G. Turrigiano and Sacha Nelson of Brandeis University, who first observed compensatory changes in excitatory postsynaptic currents (mEPSCs) after chronic activity manipulations.[6]
Mechanism
Synaptic scaling has been proposed as a potential mechanism of homeostatic plasticity.[7] Homeostatic plasticity can be used to describe a process that maintains the stability of neuronal functions through a coordinated plasticity among subcellular compartments, such as the synapses versus the neurons and the cell bodies versus the axons.[8] Recently, it was proposed that homeostatic synaptic scaling may play a role in establishing the specificity of an associative memory.[9]
Homeostatic plasticity also maintains neuronal excitability in a real-time manner through the coordinated plasticity of threshold and refractory period at voltage-gated sodium channels.[10]
Role in central pattern generators
Homeostatic plasticity is also very important in the context of central pattern generators. In this context, neuronal properties are modulated in response to environmental changes in order to maintain an appropriate neural output.[3]
References
- ↑ "Homeostatic plasticity in the developing nervous system". Nature Reviews. Neuroscience 5 (2): 97–107. February 2004. doi:10.1038/nrn1327. PMID 14735113.
- ↑ "A mechanism for homeostatic plasticity". Nature Neuroscience 7 (7): 691–692. July 2004. doi:10.1038/nn0704-691. PMID 15220926.
- ↑ 3.0 3.1 "Molecular mechanisms of homeostatic plasticity in central pattern generator networks". Developmental Neurobiology 80 (1–2): 58–69. January 2020. doi:10.1002/dneu.22727. PMID 31778295.
- ↑ 4.0 4.1 "miRNA-Dependent Control of Homeostatic Plasticity in Neurons". Frontiers in Cellular Neuroscience 13: 536. 2019. doi:10.3389/fncel.2019.00536. PMID 31866828.
- ↑ "TNF-Mediated Homeostatic Synaptic Plasticity: From in vitro to in vivo Models". Frontiers in Cellular Neuroscience 14: 565841. 2020. doi:10.3389/fncel.2020.565841. PMID 33192311.
- ↑ "Activity-dependent scaling of quantal amplitude in neocortical neurons". Nature 391 (6670): 892–896. February 1998. doi:10.1038/36103. PMID 9495341. Bibcode: 1998Natur.391..892T.
- ↑ "Homeostatic synaptic plasticity: local and global mechanisms for stabilizing neuronal function". Cold Spring Harbor Perspectives in Biology 4 (1): a005736. January 2012. doi:10.1101/cshperspect.a005736. PMID 22086977.
- ↑ "Homeostasis established by coordination of subcellular compartment plasticity improves spike encoding". Journal of Cell Science 121 (Pt 17): 2961–2971. September 2008. doi:10.1242/jcs.022368. PMID 18697837.
- ↑ "Homeostatic synaptic scaling establishes the specificity of an associative memory". Current Biology 31 (11): 2274–2285.e5. June 2021. doi:10.1016/j.cub.2021.03.024. PMID 33798429.
- ↑ "Real-time neuronal homeostasis by coordinating VGSC intrinsic properties". Biochemical and Biophysical Research Communications 387 (3): 585–589. September 2009. doi:10.1016/j.bbrc.2009.07.066. PMID 19616515.
External links
 |  |
