ArticleFrontiers in cellular neuroscience2014
Augmented Inhibition from Cannabinoid-Sensitive Interneurons Diminishes CA1 Output after Traumatic Brain Injury.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Microglia depletion improves hippocampal circuit function after mild traumatic brain injury in male mice.Brain, behavior, and immunity · 2026Article
- Neonatal microglia replacement in mice modulates seizure severity in adulthood.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Mild Traumatic Brain Injury Impairs Fear Extinction and Network Excitability in the Infralimbic Cortex.Journal of neurotrauma · 2025Article
- Cortical Morphometric Similarity Remodeling in Traumatic Brain Injury Links Cognitive Impairments with Transcriptional Changes and Type-Specific Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Enhancing cognitive recovery in chronic traumatic brain injury through simultaneous allosteric modulation of α7 nicotinic acetylcholine and α5 GABAExperimental neurology · 2024Article
- Detection and verification of neurodegeneration after traumatic brain injury in the mouse: Immunohistochemical staining for amyloid precursor protein.Brain pathology (Zurich, Switzerland) · 2023Article
- Flexibility ofFrontiers in cellular neuroscience · 2022Article
- Novel microglia-mediated mechanisms underlying synaptic loss and cognitive impairment after traumatic brain injury.Brain, behavior, and immunity · 2021Article
- Concussion increases CA1 activity during prolonged inactivity in a familiar environment.Experimental neurology · 2020Article
- Converging early responses to brain injury pave the road to epileptogenesis.Journal of neuroscience research · 2019Review
- Memory Deficit in an Object Location Task after Mild Traumatic Brain Injury Is Associated with Impaired Early Object Exploration and Both Are Restored by Branched Chain Amino Acid Dietary Therapy.Journal of neurotrauma · 2018Article
- Diminished Dentate Gyrus Filtering of Cortical Input Leads to Enhanced Area Ca3 Excitability after Mild Traumatic Brain Injury.Journal of neurotrauma · 2018Article
- Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.Current neurology and neuroscience reports · 2017Review
- A Comparison of Different Slicing Planes in Preservation of Major Hippocampal Pathway Fibers in the Mouse.Frontiers in neuroanatomy · 2017Article
- Mild Traumatic Brain Injury Decreases Broadband Power in Area CA1.Journal of neurotrauma · 2016Article
- Primary blast injury causes cognitive impairments and hippocampal circuit alterations.Experimental neurology · 2016Article
- Diminished amygdala activation and behavioral threat response following traumatic brain injury.Experimental neurology · 2016Article
- Facilitating Mitochondrial Calcium Uptake Improves Activation-Induced Cerebral Blood Flow and Behavior after mTBI.Frontiers in systems neuroscience · 2016Article
- Hippocampal Neurophysiologic Changes after Mild Traumatic Brain Injury and Potential Neuromodulation Treatment Approaches.Frontiers in systems neuroscience · 2016Review
- Brain Injury Impairs Working Memory and Prefrontal Circuit Function.Frontiers in neurology · 2015Article
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6 authors.
Funding
Abstract
The neurological impairments associated with traumatic brain injury include learning and memory deficits and increased risk of seizures. The hippocampus is critically involved in both of these phenomena and highly susceptible to damage by traumatic brain injury. To examine network activity in the hippocampal CA1 region after lateral fluid percussion injury, we used a combination of voltage-sensitive dye, field potential, and patch clamp recording in mouse hippocampal brain slices. When the stratum radiatum (SR) was stimulated in slices from injured mice, we found decreased depolarization in SR and increased hyperpolarization in stratum oriens (SO), together with a decrease in the percentage of pyramidal neurons firing stimulus-evoked action potentials. Increased hyperpolarization in SO persisted when glutamatergic transmission was blocked. However, we found no changes in SO responses when the alveus was stimulated to directly activate SO. These results suggest that the increased SO hyperpolarization evoked by SR stimulation was mediated by interneurons that have cell bodies and/or axons in SR, and form synapses in stratum pyramidale and SO. A low concentration (100 nM) of the synthetic cannabinoid WIN55,212-2, restored CA1 output in slices from injured animals. These findings support the hypothesis that increased GABAergic signaling by cannabinoid-sensitive interneurons contributes to the reduced CA1 output following traumatic brain injury.
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