CREB-Dependent Regulation of GAD65 Transcription by BDNF/TrkB in Cortical Interneurons
Abstract
In the cerebral cortex, the functional output of projection neurons is fine-tuned by inhibitory neurons present in the network, which use γ-aminobutyric acid (GABA) as their main neurotransmitter. Previous studies have suggested that the expression levels of the rate-limiting GABA synthetic enzyme, GAD65, depend on brain derived neurotrophic factor (BDNF)/TrkB activation. However, the molecular mechanisms by which this neurotrophic factor and its receptor controls GABA synthesis are still unknown. Here, we show a direct regulation of the GAD65 gene by BDNF-TrkB signaling via CREB in cortical interneurons. Conditional ablation of TrkB in cortical interneurons causes a cell-autonomous decrease in the synaptically enriched GAD65 protein and its transcripts levels, suggesting that transcriptional regulation of the GAD65 gene is altered. Dissection of the intracellular pathway that underlies this process revealed that BDNF/TrkB signaling controls the transcription of GAD65 in a Ras-ERK-CREB-dependent manner. Our study reveals a novel molecular mechanism through which BDNF/TrkB signaling may modulate the maturation and function of cortical inhibitory circuits.
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Molecular markers of synaptic potentiation like arc, BDNF or CaMKIV are involved in both the potentiation and depression of synaptic strength or other forms of non-Hebbian scaling.
“Also, molecular markers of synaptic potentiation like arc, BDNF or Calmodulin-dependent-kinase (CaMK) IV are involved in both the potentiation and depression of synaptic strength or other forms of non-Hebbian scaling (1026, 1067), questioning that the relative increase and decrease of these markers across sleep and wakefulness, respectively, is actually related to one specific form of synaptic”
From About Sleep's Role in Memory (2013) · cites this paper as [1026]
The Introduction (page unavailable) links BDNF to inhibitory-circuit plasticity, and the Discussion (page unavailable) says GAD65-dependent synaptic plasticity is modulated by BDNF. The paper also mentions impaired long-term depression when GAD65 is absent, but it does not establish that BDNF participates in both potentiation and depression or in non-Hebbian scaling; it does not address Arc or CaMKIV in that role. (LLM, conf=0.78)
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- Authors
- Sánchez-Huertas, C., & Rico, B.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Venue
- Cerebral Cortex
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-08-25
- Volume
- 21
- Issue
- 4
- Pages
- 777-788
- ISSN
- 1047-3211 (ISSN-L)
- 1460-2199
- OpenAlex
- W2027713051
- Cited by
- 96
- References
- 85
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 7 · 2023: 2 · 2022: 8 · 2021: 8 · 2020: 10 · 2019: 7 · 2018: 6 · 2017: 4 · 2016: 8 · 2015: 7 · 2014: 3 · 2013: 6 · 2012: 7
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cerebral Cortex (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- GAD65, BDNF/TrkB signaling, CREB, cortical interneurons, GABA synthesis, transcriptional regulation, inhibitory circuits
- MeSH terms
- Animals, Cerebral Cortex, Gene Expression Regulation, Glutamate Decarboxylase, Immunohistochemistry, Interneurons, Mice, Inbred C57BL, Mice, Transgenic, Transcription, Genetic, Immunoblotting, Signal Transduction, Cyclic AMP Response Element-Binding Protein, Brain-Derived Neurotrophic Factor, Reverse Transcriptase Polymerase Chain Reaction, Receptor, trkB, Chromatin Immunoprecipitation, Mice
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