ArticleBrain structure & function2019
Cortistatin-expressing interneurons require TrkB signaling to suppress neural hyper-excitability.
Article in Brain structure & function, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Resting-State Brain Activity Changes and Their Genetic Correlates in Mild Traumatic Brain Injury.Human brain mapping · 2025Pooled it
- Cortistatin neurons in the prelimbic cortex regulate seizure susceptibility in female mice via BDNF-TrkB signaling.bioRxiv : the preprint server for biology · 2026Article
- Molecular Genetics of Acquired Temporal Lobe Epilepsy.Biomolecules · 2024Review
- TrkB-dependent regulation of molecular signaling across septal cell types.Translational psychiatry · 2024Article
- The basolateral amygdala to lateral septum circuit is critical for regulating social novelty in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Genetic knockout ofFrontiers in cellular neuroscience · 2023Article
- Decoding Shared Versus Divergent Transcriptomic Signatures Across Cortico-Amygdala Circuitry in PTSD and Depressive Disorders.The American journal of psychiatry · 2022Article
- Effect and mechanism of BDNF/TrkB signaling on vestibular compensation.Bioengineered · 2021Article
- Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Signaling of brain-derived neurotrophic factor (BDNF) via tropomyosin receptor kinase B (TrkB) plays a critical role in the maturation of cortical inhibition and controls expression of inhibitory interneuron markers, including the neuropeptide cortistatin (CST). CST is expressed exclusively in a subset of cortical and hippocampal GABAergic interneurons, where it has anticonvulsant effects and controls sleep slow-wave activity (SWA). We hypothesized that CST-expressing interneurons play a critical role in regulating excitatory/inhibitory balance, and that BDNF, signaling through TrkB receptors on CST-expressing interneurons, is required for this function. Ablation of CST-expressing cells caused generalized seizures and premature death during early postnatal development, demonstrating a critical role for these cells in providing inhibition. Mice in which TrkB was selectively deleted from CST-expressing interneurons were hyperactive, slept less and developed spontaneous seizures. Frequencies of spontaneous excitatory post-synaptic currents (sEPSCs) on CST-expressing interneurons were attenuated in these mice. These data suggest that BDNF, signaling through TrkB receptors on CST-expressing cells, promotes excitatory drive onto these cells. Loss of excitatory drive onto CST-expressing cells that lack TrkB receptors may contribute to observed hyperexcitability and epileptogenesis.
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Registered trials
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