Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity
Dynamic reorganization of neural circuits can occur through the selective strengthening of synapses between neurons that are coactive in response to the encoded information (Shatz, 1990). However, the positive feedback resulting from synaptic strengthening and neuronal coactivity can lead to the des...
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| Format: | Article |
| Language: | en_US |
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Frontiers Research Foundation
2015
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| Online Access: | http://hdl.handle.net/1721.1/99678 |
| _version_ | 1826209749355462656 |
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| author | Subramanian, Jaichandar Dickman, Dion |
| author2 | Picower Institute for Learning and Memory |
| author_facet | Picower Institute for Learning and Memory Subramanian, Jaichandar Dickman, Dion |
| author_sort | Subramanian, Jaichandar |
| collection | MIT |
| description | Dynamic reorganization of neural circuits can occur through the selective strengthening of synapses between neurons that are coactive in response to the encoded information (Shatz, 1990). However, the positive feedback resulting from synaptic strengthening and neuronal coactivity can lead to the destabilization of neuronal networks. Thus, synapses must maintain the capacity for change necessary for learning and memory, yet constrain this inherently destabilizing flexibility to enable stable neural function throughout life. Evidence has emerged in recent years that activity within neural circuits can shape the synaptic properties of component neurons in a manner that maintains stable excitatory drive, a process referred to as homeostatic synaptic plasticity (Turrigiano and Nelson, 2000; Pozo and Goda, 2010; Davis, 2013). Potent and adaptive homeostatic mechanisms have been demonstrated in a variety of systems to modulate activity at the level of an individual neuron, synapse, circuit, or entire network, and dysregulation at some or all of these levels may contribute to neuropsychiatric disorders, intellectual disability, and epilepsy (Wondolowski and Dickman, 2013). Greater mechanistic understanding of homeostatic plasticity will provide key insights into the etiology of these disorders, which may result from network instability and synaptic dysfunction. Over the past 15 years, the molecular mechanisms of this form of plasticity have been intensely studied in various model organisms, including invertebrates and vertebrates (Davis and Müller, 2015). Though, once thought to have a predominantly postsynaptic basis, emerging evidence suggests that homeostatic mechanisms act on both sides of the synapse, through mechanisms such as retrograde signaling, to orchestrate compensatory adaptations that maintain stable network function (Vitureira et al., 2012). These trans-synaptic signaling systems ultimately alter neurotransmitter release probability by a variety of mechanisms including changes in vesicle pool size and calcium influx (Davis and Müller, 2015). These adaptations are not expected to occur homogenously at all terminals of a pre-synaptic neuron, as they might synapse with neurons in non-overlapping circuits. However, the factors that govern the homeostatic control of synapse-specific plasticity are only beginning to be understood. |
| first_indexed | 2024-09-23T14:28:35Z |
| format | Article |
| id | mit-1721.1/99678 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T14:28:35Z |
| publishDate | 2015 |
| publisher | Frontiers Research Foundation |
| record_format | dspace |
| spelling | mit-1721.1/996782022-10-01T21:27:45Z Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity Subramanian, Jaichandar Dickman, Dion Picower Institute for Learning and Memory Subramanian, Jaichandar Dynamic reorganization of neural circuits can occur through the selective strengthening of synapses between neurons that are coactive in response to the encoded information (Shatz, 1990). However, the positive feedback resulting from synaptic strengthening and neuronal coactivity can lead to the destabilization of neuronal networks. Thus, synapses must maintain the capacity for change necessary for learning and memory, yet constrain this inherently destabilizing flexibility to enable stable neural function throughout life. Evidence has emerged in recent years that activity within neural circuits can shape the synaptic properties of component neurons in a manner that maintains stable excitatory drive, a process referred to as homeostatic synaptic plasticity (Turrigiano and Nelson, 2000; Pozo and Goda, 2010; Davis, 2013). Potent and adaptive homeostatic mechanisms have been demonstrated in a variety of systems to modulate activity at the level of an individual neuron, synapse, circuit, or entire network, and dysregulation at some or all of these levels may contribute to neuropsychiatric disorders, intellectual disability, and epilepsy (Wondolowski and Dickman, 2013). Greater mechanistic understanding of homeostatic plasticity will provide key insights into the etiology of these disorders, which may result from network instability and synaptic dysfunction. Over the past 15 years, the molecular mechanisms of this form of plasticity have been intensely studied in various model organisms, including invertebrates and vertebrates (Davis and Müller, 2015). Though, once thought to have a predominantly postsynaptic basis, emerging evidence suggests that homeostatic mechanisms act on both sides of the synapse, through mechanisms such as retrograde signaling, to orchestrate compensatory adaptations that maintain stable network function (Vitureira et al., 2012). These trans-synaptic signaling systems ultimately alter neurotransmitter release probability by a variety of mechanisms including changes in vesicle pool size and calcium influx (Davis and Müller, 2015). These adaptations are not expected to occur homogenously at all terminals of a pre-synaptic neuron, as they might synapse with neurons in non-overlapping circuits. However, the factors that govern the homeostatic control of synapse-specific plasticity are only beginning to be understood. National Institutes of Health (U.S.) (Grant NS019546) 2015-11-03T17:09:33Z 2015-11-03T17:09:33Z 2015-09 2015-07 Article http://purl.org/eprint/type/JournalArticle 1662-5102 http://hdl.handle.net/1721.1/99678 Subramanian, Jaichandar, and Dion Dickman. “Editorial: Homeostatic and Retrograde Signaling Mechanisms Modulating Presynaptic Function and Plasticity.” Front. Cell. Neurosci. 9 (September 30, 2015). en_US http://dx.doi.org/10.3389/fncel.2015.00380 Frontiers in Cellular Neuroscience Creative Commons Attribution http://creativecommons.org/licenses/by/4.0/ application/pdf Frontiers Research Foundation Frontiers Research Foundation |
| spellingShingle | Subramanian, Jaichandar Dickman, Dion Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| title | Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| title_full | Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| title_fullStr | Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| title_full_unstemmed | Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| title_short | Editorial: Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| title_sort | editorial homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity |
| url | http://hdl.handle.net/1721.1/99678 |
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