ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Decrease in tonic inhibition contributes to increase in dentate semilunar granule cell excitability after brain injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 120 citations in OpenAlex.
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury.Journal of neuroinflammation · 2026Article
- Multiplexed changes in synaptic transmission underlie stress-induced reduction of persistent firing in the parietal cortex.Progress in neurobiology · 2026Article
- Altered Physiology and Ensemble Recruitment of Dentate Gyrus Semilunar Granule Cells in a Mouse Model of Epilepsy.bioRxiv : the preprint server for biology · 2026Article
- Neuronal Toll-like Receptor-4 regulation of Matrix Metalloproteinase-9 Activity Mediates Dentate Circuit Dysfunction after Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Longitudinal Effects of Mild Traumatic Brain Injury on the Gut Microbiome and Acoustic Startle Response in Male and Female Rats.Journal of neurotrauma · 2026Article
- Perisomatic innervation on the semilunar granule cells and outer molecular layer granule cells of the dentate gyrus of the mouse.Frontiers in neuroanatomy · 2026Article
- Article
- Differential Glutamatergic Inputs to Semilunar Granule Cells and Granule Cells Underscore Dentate Gyrus Projection Neuron Diversity.bioRxiv : the preprint server for biology · 2025Article
- Medial ganglionic eminence transplantation restores inhibition after central visual system brain injury.PNAS nexus · 2025Article
- Insights into epileptogenesis from post-traumatic epilepsy.Nature reviews. Neurology · 2024Review
- Reclusive chandeliers: Functional isolation of dentate axo-axonic cells after experimental status epilepticus.Progress in neurobiology · 2023Article
- Early deficits in dentate circuit and behavioral pattern separation after concussive brain injury.Experimental neurology · 2023Article
- RECLUSIVE CHANDELIERS: FUNCTIONAL ISOLATION OF DENTATE AXO-AXONIC CELLS AFTER EXPERIMENTAL STATUS EPILEPTICUS.bioRxiv : the preprint server for biology · 2023Article
- Mild Traumatic Brain Injury Affects Orexin/Hypocretin Physiology Differently in Male and Female Mice.Journal of neurotrauma · 2023Article
- Differential expression of GABAFrontiers in cellular neuroscience · 2023Article
- Article
- Somatostatin interneurons exhibit enhanced functional output and resilience to axotomy after mild traumatic brain injury.Neurobiology of disease · 2022Article
- Adaptive Mossy Cell Circuit Plasticity after Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
17 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain injury is an etiological factor for temporal lobe epilepsy and can lead to memory and cognitive impairments. A recently characterized excitatory neuronal class in the dentate molecular layer, semilunar granule cell (SGC), has been proposed to regulate dentate network activity patterns and working memory formation. Although SGCs, like granule cells, project to CA3, their typical sustained firing and associational axon collaterals suggest that they are functionally distinct from granule cells. We find that brain injury results in an enhancement of SGC excitability associated with an increase in input resistance 1 week after trauma. In addition to prolonging miniature and spontaneous IPSC interevent intervals, brain injury significantly reduces the amplitude of tonic GABA currents in SGCs. The postinjury decrease in SGC tonic GABA currents is in direct contrast to the increase observed in granule cells after trauma. Although our observation that SGCs express Prox1 indicates a shared lineage with granule cells, data from control rats show that SGC tonic GABA currents are larger and sIPSC interevent intervals shorter than in granule cells, demonstrating inherent differences in inhibition between these cell types. GABA(A) receptor antagonists selectively augmented SGC input resistance in controls but not in head-injured rats. Moreover, post-traumatic differences in SGC firing were abolished in GABA(A) receptor blockers. Our data show that cell-type-specific post-traumatic decreases in tonic GABA currents boost SGC excitability after brain injury. Hyperexcitable SGCs could augment dentate throughput to CA3 and contribute substantively to the enhanced risk for epilepsy and memory dysfunction after traumatic brain injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.