Increased hippocampal GABAergic inhibition after long-term high-intensity sound exposure

PLoS One. 2019 May 8;14(5):e0210451. doi: 10.1371/journal.pone.0210451. eCollection 2019.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acoustic Stimulation*
  • Animals
  • CA1 Region, Hippocampal / physiology
  • GABAergic Neurons / metabolism*
  • Glutamates / metabolism
  • Hippocampus / physiology*
  • Long-Term Potentiation*
  • Male
  • Neural Inhibition*
  • Pyramidal Cells / metabolism*
  • Rats
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Sound*

Substances

  • Glutamates
  • Receptors, N-Methyl-D-Aspartate

Grants and funding

This work was supported by FAPESP grants 2016/01607-4 (RML) and 2015/22327-7 (AOSC). R.M.L. is a CNPq Research Fellow.