Electrophysiological monitoring of hearing function during cochlear perilymphatic perfusions

Abstract Conclusion: The cochlear perilymphatic perfusion produces, by itself, significant effects in the cochlear physiology that could be associated with the surgical procedure. These effects need to be well characterized to allow a reliable quantification of the effects of the experimental agent being tested. Objectives: The study focused on the accurate description of the electrophysiological effects on the cochlear potential recordings of perilymphatic perfusions. Methods: Two successive cochlear perilymphatic perfusions were carried out. The first used artificial perilymph. The second used artificial perilymph alone or a kainic acid (KA) solution in artificial perilymph. The compound action potential of the auditory nerve (CAP-AN) was recorded: (1) before the first perfusion, (2) after the first perfusion and (3) after the second perfusion, and compared between groups. Results: The first intracochlear perfusion with artificial perilymph produced significant effects in the CAP-AN that could be related to the surgical procedure. These effects were analysed separately from the effects produced by the KA. In particular, the KA administered intracochlearly produced a significant increase in the latency and a decrease in the amplitude of the CAP-AN N1 wave compared with the controls that were perfused twice with artificial perilymph.

[1]  C. Mulle,et al.  Kainate receptors in epilepsy and excitotoxicity , 2009, Neuroscience.

[2]  R. Bobbin.  Glutamate and aspartate mimic the afferent transmitter in the cochlea , 1979, Experimental Brain Research.

[3]  R. Pujol,et al.  Neurotoxicity of kainic acid in the rat cochlea during early developmental stages , 2004, European Archives of Oto-Rhino-Laryngology.

[4]  F. Carricondo,et al.  Sensitivity to glutamate neurotoxicity in different developmental periods of the rat cochlea. , 2002, Advances in oto-rhino-laryngology.

[5]  F. Carricondo,et al.  Cochlear Microphonic Potentials: A New Recording Technique , 2001, The Annals of otology, rhinology, and laryngology.

[6]  Á. Merchán-Pérez,et al.  Decalcification by ascorbic acid for immuno- and affinohistochemical techniques on the inner ear , 1999, Histochemistry and Cell Biology.

[7]  F. Carricondo,et al.  Trimetazidine prevents cochlear lesions induced by intraperitoneal and perilymphatic administration of kainic acid , 1999, Brain Research.

[8]  R. Salvi,et al.  Effects of kainic acid on the cochlear potentials and distortion product otoacoustic emissions in chinchilla , 1996, Hearing Research.

[9]  J. Puel.  Chemical synaptic transmission in the cochlea , 1995, Progress in Neurobiology.

[10]  P. Gil-Loyzaga.  Neurotransmitters of the olivocochlear lateral efferent system: with an emphasis on dopamine. , 1995, Acta oto-laryngologica.

[11]  H. Cousillas,et al.  Effects of noise stimulation on cochlear dopamine metabolism , 1993, Brain Research.

[12]  M. J. Hernández-Ortiz,et al.  Diltiazem protects against neurotoxicity induced by excitotoxic amino acids on cochlear afferent fibers. , 1993, ORL; journal for oto-rhino-laryngology and its related specialties.

[13]  R. Wenthold,et al.  Immunocytochemical localization of glutamate immunoreactivity in the guinea pig cochlea , 1989, Hearing Research.

[14]  B. M. Johnstone,et al.  Kainic acid selectively alters auditory dendrites connected with cochlear inner hair cells , 1985, Hearing Research.

[15]  R. Pujol,et al.  A radioautographic study of [3H] l-glutamate and [3H] l-glutamine uptake in the guinea-pig cochlea , 1983, Neuroscience.

[16]  P. Hamrick,et al.  Ion transport in guinea pig cochlea. I. Potassium and sodium transport. , 1978, Acta oto-laryngologica.

[17]  D. A. Godfrey,et al.  Levels of putative transmitter amino acids in the guinea pig cochlea. , 1976, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.