Change in gene expression levels of GABA, glutamate and neurosteroid pathways due to acoustic trauma in the cochlea

Cerrah Gunes M., Gunes M. S., Vural A., Aybuga F., Bayram A., Bayram K. K., ...More

JOURNAL OF NEUROGENETICS, vol.35, no.1, pp.45-57, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 35 Issue: 1
  • Publication Date: 2021
  • Doi Number: 10.1080/01677063.2021.1904922
  • Journal Name: JOURNAL OF NEUROGENETICS
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, EMBASE, MEDLINE
  • Page Numbers: pp.45-57
  • Erciyes University Affiliated: Yes

Abstract

The characteristic feature of noise-induced hearing loss (NIHL) is the loss or malfunction of the outer hair cells (OHC) and the inner hair cells (IHC) of the cochlea. 90-95% of the spiral ganglion neurons, forming the cell bodies of cochlear nerve, synapse with the IHCs. Glutamate is the most potent excitatory neurotransmitter for IHC-auditory nerve synapses. Excessive release of glutamate in response to acoustic trauma (AT), may cause excitotoxicity by causing damage to the spiral ganglion neurons (SGN) or loss of the spiral ganglion dendrites, post-synaptic to the IHCs. Another neurotransmitter, GABA, plays an important role in the processing of acoustic stimuli and central regulation after peripheral injury, so it is potentially related to the regulation of hearing function and sensitivity after noise. The aim of this study is to evaluate the effect of AT on the expressions of glutamate excitotoxicity, GABA inhibition and neurosteroid synthesis genes.