ArticlePloS one2014
Reduced GABAergic inhibition in the basolateral amygdala and the development of anxiety-like behaviors after mild traumatic brain injury.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Incidence of anxiety after traumatic brain injury: a systematic review and meta-analysis.BMC neurology · 2024Pooled it
- Connectivity differences between Gulf War Illness (GWI) phenotypes during a test of attention.PloS one · 2019Trial
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Impact of serotonin transporter deficiency on parvalbumin- and neuropeptide Y-producing neurons of the lateral and basolateral amygdalar nuclei.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Deep cerebellar stimulation restores chronic motor deficits and loss of GABAergic neurons following sensorimotor cortex surgical brain injury in female rats.Experimental neurology · 2026Article
- Neuroprotective mechanism of syringic acid targeting oxidative damage and neuroinflammation in an experimental model of traumatic brain injury.Inflammopharmacology · 2026Article
- Behavioral deficits after traumatic brain injury: Neuroprotective effect of Diosmin.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Advances and challenges in experimental models of posttraumatic epilepsy for therapeutic interventions.Pharmacological reviews · 2025Review
- Review
- Non-invasive therapeutics for neurotrauma: a mechanistic overview.Frontiers in neurology · 2025Review
- Enhancing cognitive recovery in chronic traumatic brain injury through simultaneous allosteric modulation of α7 nicotinic acetylcholine and α5 GABAExperimental neurology · 2024Article
- Enhancing cognitive function in chronic TBI: The Role of α7 nicotinic acetylcholine receptor modulation.Experimental neurology · 2024Article
- Neurobehavioral and inflammatory responses following traumatic brain injury in male and female mice.Behavioural brain research · 2024Article
- A novel anxiety-associated SNP identified inFrontiers in behavioral neuroscience · 2024Article
- Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders.Frontiers in neuroscience · 2024Review
- Emotional Regulation and Adolescent Concussion: Overview and Role of Neuroimaging.International journal of environmental research and public health · 2023Review
- Alpha-linolenic acid enhances the facilitation of GABAergic neurotransmission in the BLA and CA1.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Exposure to Juvenile Stress Induces Epigenetic Alterations in the GABAergic System in Rats.Genes · 2023Article
- Examining the long-term effects of traumatic brain injury on fear extinction in male rats.Frontiers in behavioral neuroscience · 2023Article
- GABAergic circuits of the basolateral amygdala and generation of anxiety after traumatic brain injury.Amino acids · 2022Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a major public health concern affecting a large number of athletes and military personnel. Individuals suffering from a TBI risk developing anxiety disorders, yet the pathophysiological alterations that result in the development of anxiety disorders have not yet been identified. One region often damaged by a TBI is the basolateral amygdala (BLA); hyperactivity within the BLA is associated with increased expression of anxiety and fear, yet the functional alterations that lead to BLA hyperexcitability after TBI have not been identified. We assessed the functional alterations in inhibitory synaptic transmission in the BLA and one mechanism that modulates excitatory synaptic transmission, the α7 containing nicotinic acetylcholine receptor (α7-nAChR), after mTBI, to shed light on the mechanisms that contribute to increased anxiety-like behaviors. Seven and 30 days after a mild controlled cortical impact (CCI) injury, animals displayed significantly greater anxiety-like behavior. This was associated with a significant loss of GABAergic interneurons and significant reductions in the frequency and amplitude of spontaneous and miniature GABAA-receptor mediated inhibitory postsynaptic currents (IPSCs). Decreases in the mIPSC amplitude were associated with reduced surface expression of α1, β2, and γ2 GABAA receptor subunits. However, significant increases in the surface expression and current mediated by α7-nAChR, were observed, signifying increases in the excitability of principal neurons within the BLA. These results suggest that mTBI causes not only a significant reduction in inhibition in the BLA, but also an increase in neuronal excitability, which may contribute to hyperexcitability and the development of anxiety disorders.
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Registered trials
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.