ArticleMolecular neurobiology2020
The Recovery of GABAergic Function in the Hippocampus CA1 Region After mTBI.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- α-linolenic acid-induced facilitation of GABAergic synaptic transmission is mediated via acid-sensing ion channel (ASIC1a) activity in the basolateral amygdala.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Advantages of nanocarriers for basic research in the field of traumatic brain injury.Neural regeneration research · 2024Review
- Hippocampal interneuronal dysfunction and hyperexcitability in a porcine model of concussion.Communications biology · 2023Article
- Alpha-linolenic acid enhances the facilitation of GABAergic neurotransmission in the BLA and CA1.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- GABAInternational journal of molecular sciences · 2022Article
- Teasing apart trauma: neural oscillations differentiate individual cases of mild traumatic brain injury from post-traumatic stress disorder even when symptoms overlap.Translational psychiatry · 2021Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major public health concern in the USA. There are approximately 2.5 million brain injuries annually, 90% of which may be classified as mild since these individuals do not display clear morphological abnormalities following injury on imaging. The majority of individuals develop neurocognitive deficits such as learning and memory impairment and recovery occurs over 3 to 6 months after mild TBI (mTBI). The hippocampus is highly susceptible to injury from mTBI due to the anatomic localization and has been implicated in the neurocognitive impairments after mTBI. Here, we investigated whether the mTBI-induced morphological and pathophysiological alterations of GABAergic interneurons in the CA1 subfield of the hippocampus recovers after 30 days in the controlled cortical impact (CCI) model of TBI. Design-based stereology shows a significant reduction in the number of GABAergic interneurons 7 days after CCI. However, the number of GABAergic interneurons is not significantly reduced at 30 days after CCI. The total number of neurons is not altered over the course of 30 days. GABAergic inhibitory currents in the CA1 subfield also show that, although there is a significant reduction in the CCI group at 7 days, the currents are not significantly different from sham controls at 30 days. We suggest that the recovery of GABAergic function in the CA1 subfield of the hippocampus observed 30 days after CCI is one of the mechanisms associated with the recovery of memory after mTBI.
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