ArticlePloS one2019
Increased hippocampal GABAergic inhibition after long-term high-intensity sound exposure.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Neuroplasticity and tinnitus: the role of Brain-Derived Neurotrophic Factor in pathogenesis and treatment.Frontiers in neuroscience · 2025Review
- Targeting the Limbic System: Insights into Its Involvement in Tinnitus.International journal of molecular sciences · 2023Review
- Noise as a cause of neurodegenerative disorders: molecular and cellular mechanisms.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Loss of Brain-Derived Neurotrophic Factor Mediates Inhibition of Hippocampal Long-Term Potentiation by High-Intensity Sound.Cellular and molecular neurobiology · 2021Article
- Plasticity in Limbic Regions at Early Time Points in Experimental Models of Tinnitus.Frontiers in systems neuroscience · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to loud sounds is related to harmful mental and systemic effects. The hippocampal function can be affected to either high-intensity sound exposure or long-term sound deprivation. We previously showed that hippocampal long-term potentiation (LTP) is inhibited after ten days of daily exposure to 2 minutes of high-intensity noise (110 dB), in the hippocampi of Wistar rats. Here we investigated how the glutamatergic and GABAergic neurotransmission mediated by ionotropic receptors is affected by the same protocol of high-intensity sound exposure. We found that while the glutamatergic transmission both by AMPA/kainate and NMDA receptors in the Schaffer-CA1 synapses is unaffected by long-term exposure to high-intensity sound, the amplitude of the inhibitory GABAergic currents is potentiated, but not the frequency of both spontaneous and miniature currents. We conclude that after prolonged exposure to short periods of high-intensity sound, GABAergic transmission is potentiated in the hippocampal CA1 pyramidal neurons. This effect could be an essential factor for the reduced LTP in the hippocampi of these animals after high-intensity sound exposure. We conclude that prolonged exposure to high- intensity sound could affect hippocampal inhibitory transmission and consequently, its function.
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