The Type 2 Diabetes Factor Methylglyoxal Mediates Axon Initial Segment Shortening and Alters Neuronal Function at the Cellular and Network Levels Article Swipe
Ryan B. Griggs
,
Duc V.M. Nguyen
,
Leonid M. Yermakov
,
Jeneane M. Jaber
,
Jennae N. Shelby
,
Josef K. Steinbrunner
,
John A. Miller
,
Carlos Gonzalez‐Islas
,
Peter Wenner
,
Keiichiro Susuki
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1523/eneuro.0201-21.2021
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1523/eneuro.0201-21.2021
Recent evidence suggests that alteration of axon initial segment (AIS) geometry (i.e., length or location along the axon) contributes to CNS dysfunction in neurological diseases. For example, AIS length is shorter in the prefrontal cortex of type 2 diabetic mice with cognitive impairment. To determine the key type 2 diabetes-related factor that produces AIS shortening we modified levels of insulin, glucose, or the reactive glucose metabolite methylglyoxal in cultures of dissociated cortices from male and female mice and quantified AIS geometry using immunofluorescent imaging of the AIS proteins AnkyrinG and βIV spectrin. Neither insulin nor glucose modification altered AIS length. Exposure to 100 but not 1 or 10 μ m methylglyoxal for 24 h resulted in accumulation of the methylglyoxal-derived advanced glycation end-product hydroimidazolone and produced reversible AIS shortening without cell death. Methylglyoxal-evoked AIS shortening occurred in both excitatory and putative inhibitory neuron populations and in the presence of tetrodotoxin (TTX). In single-cell recordings resting membrane potential was depolarized at 0.5–3 h and returned to normal at 24 h. In multielectrode array (MEA) recordings methylglyoxal produced an immediate ∼300% increase in spiking and bursting rates that returned to normal within 2 min, followed by a ∼20% reduction of network activity at 0.5–3 h and restoration of activity to baseline levels at 24 h. AIS length was unchanged at 0.5–3 h despite the presence of depolarization and network activity reduction. Nevertheless, these results suggest that methylglyoxal could be a key mediator of AIS shortening and disruptor of neuronal function during type 2 diabetes.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1523/eneuro.0201-21.2021
- https://www.eneuro.org/content/eneuro/8/5/ENEURO.0201-21.2021.full.pdf
- OA Status
- gold
- Cited By
- 4
- References
- 92
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3199055078
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Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W3199055078Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1523/eneuro.0201-21.2021Digital Object Identifier
- Title
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The Type 2 Diabetes Factor Methylglyoxal Mediates Axon Initial Segment Shortening and Alters Neuronal Function at the Cellular and Network LevelsWork title
- Type
-
articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2021Year of publication
- Publication date
-
2021-09-01Full publication date if available
- Authors
-
Ryan B. Griggs, Duc V.M. Nguyen, Leonid M. Yermakov, Jeneane M. Jaber, Jennae N. Shelby, Josef K. Steinbrunner, John A. Miller, Carlos Gonzalez‐Islas, Peter Wenner, Keiichiro SusukiList of authors in order
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https://doi.org/10.1523/eneuro.0201-21.2021Publisher landing page
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https://www.eneuro.org/content/eneuro/8/5/ENEURO.0201-21.2021.full.pdfDirect link to full text PDF
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-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
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https://www.eneuro.org/content/eneuro/8/5/ENEURO.0201-21.2021.full.pdfDirect OA link when available
- Concepts
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Methylglyoxal, Chemistry, Internal medicine, Endocrinology, Axon, Neuroscience, Depolarization, Inhibitory postsynaptic potential, Biology, Biophysics, Biochemistry, Medicine, EnzymeTop concepts (fields/topics) attached by OpenAlex
- Cited by
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4Total citation count in OpenAlex
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2023: 2, 2022: 1, 2021: 1Per-year citation counts (last 5 years)
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92Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.prefrontal | 34 |
| abstract_inverted_index.quantified | 79 |
| abstract_inverted_index.recordings | 154, 174 |
| abstract_inverted_index.reduction. | 229 |
| abstract_inverted_index.reversible | 127 |
| abstract_inverted_index.shortening | 55, 129, 135, 243 |
| abstract_inverted_index.contributes | 19 |
| abstract_inverted_index.depolarized | 159 |
| abstract_inverted_index.dissociated | 71 |
| abstract_inverted_index.dysfunction | 22 |
| abstract_inverted_index.end-product | 123 |
| abstract_inverted_index.impairment. | 43 |
| abstract_inverted_index.populations | 144 |
| abstract_inverted_index.restoration | 205 |
| abstract_inverted_index.single-cell | 153 |
| abstract_inverted_index.accumulation | 117 |
| abstract_inverted_index.modification | 97 |
| abstract_inverted_index.neurological | 24 |
| abstract_inverted_index.tetrodotoxin | 150 |
| abstract_inverted_index.Nevertheless, | 230 |
| abstract_inverted_index.methylglyoxal | 67, 111, 175, 235 |
| abstract_inverted_index.depolarization | 225 |
| abstract_inverted_index.multielectrode | 171 |
| abstract_inverted_index.diabetes-related | 50 |
| abstract_inverted_index.hydroimidazolone | 124 |
| abstract_inverted_index.immunofluorescent | 83 |
| abstract_inverted_index.Methylglyoxal-evoked | 133 |
| abstract_inverted_index.methylglyoxal-derived | 120 |
| cited_by_percentile_year.max | 96 |
| cited_by_percentile_year.min | 89 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 10 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.75 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.60507968 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |