Ca2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism
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CREB is a transcription factor implicated in the control of adaptive neuronal responses. Although one function of CREB in neurons is believed to be the regulation of genes whose products control synaptic function, the targets of CREB that mediate synaptic function have not yet been identified. This report describes experiments demonstrating that CREB or a closely related protein mediates Ca2+-dependent regulation of BDNF, a neurotrophin that modulates synaptic activity. In cortical neurons, Ca2+ influx triggers phosphorylation of CREB, which by binding to a critical Ca2+ response element (CRE) within the BDNF gene activates BDNF transcription. Mutation of the BDNF CRE or an adjacent novel regulatory element as well as a blockade of CREB function resulted in a dramatic loss of BDNF transcription. These findings suggest that a CREB family member acts cooperatively with an additional transcription factor(s) to regulate BDNF transcription. We conclude that the BDNF gene is a CREB family target whose protein product functions at synapses to control adaptive neuronal responses.
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BDNF transcription is dependent on Ca2+ mediated activation of CREB.
“BDNF transcription is dependent on Ca2+ mediated activation of cAMP-response element-binding protein (CREB; Tao et al., 1998).”
From miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A (2020) · cites this paper as Tao et al., 1998
BDNF promoter I is more responsive to neuronal activity and induces activity-dependent expression of BDNF in vitro and in vivo.
“Promoter I is more responsive to neuronal activity and induces activity-dependent expression of BDNF in vitro and in vivo.”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [37]
Reelin-mediated enhancement induces activation of CREB, which increases expression of BDNF.
“Reelin-mediated enhancement induces the activation of CREB (29) (Fig. 2B, 1), which increases the expression of BDNF (45) (Fig. 2B, 2).”
From Reelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses (2017) · cites this paper as [45]
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- Authors
- Tao, X., Finkbeiner, S., Arnold, D. B., Shaywitz, A. J., & Greenberg, M. E.
- Affiliations
- Harvard University (US)
- Boston Children's Hospital (US)
- Corresponding author
- Greenberg, Michael E.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1998-04
- Volume
- 20
- Issue
- 4
- Pages
- 709-726
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W1992529363
- Cited by
- 1,561
- References
- 5
- Citations by year
- 2026: 36 · 2025: 41 · 2024: 36 · 2023: 51 · 2022: 42 · 2021: 49 · 2020: 58 · 2019: 48 · 2018: 57 · 2017: 72 · 2016: 69 · 2015: 61 · 2014: 59 · 2013: 66 · 2012: 63
- FWCI
- 23.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k08ns001817-02)
- National Institute of Neurological Disorders and Stroke (K08 NS01817, NS288829)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD018655, P30HD-18655)
- 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 › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- brain-derived neurotrophic factor, CREB, calcium influx, transcriptional regulation, CREB phosphorylation, cortical neurons, synaptic plasticity, neurotrophins, transcription factor cooperativity
- MeSH terms
- Animals, Base Sequence, Calcium, Cells, Cultured, Cerebral Cortex, Embryo, Mammalian, Exons, Gene Expression Regulation, Kinetics, Neurons, Phosphorylation, Recombinant Fusion Proteins, Regulatory Sequences, Nucleic Acid, Synapses, Transcription Factors, Transcription, Genetic, Transfection, Calcium Channels, Signal Transduction, Polymerase Chain Reaction, Mutagenesis, Site-Directed, Cyclic AMP Response Element-Binding Protein, DNA Primers, Brain-Derived Neurotrophic Factor, Biolistics, Calcium Channels, L-Type, Rats
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