Disruption of NMDAR Function Prevents Normal Experience-Dependent Homeostatic Synaptic Plasticity in Mouse Primary Visual Cortex Article Swipe
Gabriela Rodrı́guez
,
Lukas Mesik
,
Ming Gao
,
Samuel Parkins
,
Rinki Saha
,
Hey‐Kyoung Lee
·
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1523/jneurosci.2117-18.2019
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1523/jneurosci.2117-18.2019
Homeostatic regulation of synaptic strength allows for maintenance of neural activity within a dynamic range for proper circuit function. There are largely two distinct modes of synaptic plasticity that allow for homeostatic adaptation of cortical circuits: synaptic scaling and sliding threshold (BCM theory). Previous findings suggest that the induction of synaptic scaling is not prevented by blocking NMDARs, whereas the sliding threshold model posits that the synaptic modification threshold of LTP and LTD readjusts with activity and thus the outcome of synaptic plasticity is NMDAR dependent. Although synaptic scaling and sliding threshold have been considered two distinct mechanisms, there are indications from recent studies that these two modes of homeostatic plasticity may interact or that they may operate under two distinct activity regimes. Here, we report using both sexes of mouse that acute genetic knock-out of the obligatory subunit of NMDAR or acute pharmacological block of NMDAR prevents experience-dependent homeostatic regulation of AMPAR-mediated miniature EPSCs in layer 2/3 of visual cortex. This was not due to gross changes in postsynaptic neuronal activity with inhibiting NMDAR function as determine by c-Fos expression and two-photon Ca 2+ imaging in awake mice. Our results suggest that experience-dependent homeostatic regulation of intact cortical circuits is mediated by NMDAR-dependent plasticity mechanisms, which supports a sliding threshold model of homeostatic adaptation. SIGNIFICANCE STATEMENT Prolonged changes in sensory experience lead to homeostatic adaptation of excitatory synaptic strength in sensory cortices. Both sliding threshold and synaptic scaling models can account for the observed homeostatic synaptic plasticity. Here we report that visual experience-dependent homeostatic plasticity of excitatory synapses observed in superficial layers of visual cortex is dependent on NMDAR function. In particular, both strengthening of synapses induced by visual deprivation and the subsequent weakening by reinstatement of visual experience were prevented in the absence of functional NMDARs. Our results suggest that sensory experience-dependent homeostatic adaptation depends on NMDARs, which supports the sliding threshold model of plasticity and input-specific homeostatic control observed in vivo .
Related Topics
Concepts
Homeostatic plasticity
Synaptic scaling
Neuroscience
Metaplasticity
Synaptic plasticity
Nonsynaptic plasticity
NMDA receptor
Synaptic fatigue
Synaptic augmentation
Excitatory postsynaptic potential
Homeostasis
Biology
Neuroplasticity
Inhibitory postsynaptic potential
Cell biology
Receptor
Biochemistry
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1523/jneurosci.2117-18.2019
- https://www.jneurosci.org/content/jneuro/39/39/7664.full.pdf
- OA Status
- bronze
- Cited By
- 27
- References
- 52
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2967951229
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W2967951229Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1523/jneurosci.2117-18.2019Digital Object Identifier
- Title
-
Disruption of NMDAR Function Prevents Normal Experience-Dependent Homeostatic Synaptic Plasticity in Mouse Primary Visual CortexWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2019Year of publication
- Publication date
-
2019-08-14Full publication date if available
- Authors
-
Gabriela Rodrı́guez, Lukas Mesik, Ming Gao, Samuel Parkins, Rinki Saha, Hey‐Kyoung LeeList of authors in order
- Landing page
-
https://doi.org/10.1523/jneurosci.2117-18.2019Publisher landing page
- PDF URL
-
https://www.jneurosci.org/content/jneuro/39/39/7664.full.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
- OA URL
-
https://www.jneurosci.org/content/jneuro/39/39/7664.full.pdfDirect OA link when available
- Concepts
-
Homeostatic plasticity, Synaptic scaling, Neuroscience, Metaplasticity, Synaptic plasticity, Nonsynaptic plasticity, NMDA receptor, Synaptic fatigue, Synaptic augmentation, Excitatory postsynaptic potential, Homeostasis, Biology, Neuroplasticity, Inhibitory postsynaptic potential, Cell biology, Receptor, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
27Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 1, 2024: 4, 2023: 4, 2022: 9, 2021: 5Per-year citation counts (last 5 years)
- References (count)
-
52Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.postsynaptic | 169 |
| abstract_inverted_index.reinstatement | 286 |
| abstract_inverted_index.strengthening | 274 |
| abstract_inverted_index.AMPAR-mediated | 152 |
| abstract_inverted_index.input-specific | 318 |
| abstract_inverted_index.NMDAR-dependent | 203 |
| abstract_inverted_index.pharmacological | 143 |
| abstract_inverted_index.experience-dependent | 148, 193, 253, 303 |
| cited_by_percentile_year.max | 99 |
| cited_by_percentile_year.min | 89 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 6 |
| citation_normalized_percentile.value | 0.85866746 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |