Effects of a calcium channel blocker on spontaneous neural noise and gross action potential waveforms in the guinea pig cochlea

• Published in: Hearing research Vol. 188; no. 1; pp. 117 - 125
• Main Authors: Sueta, T., Zhang, S.Y., Sellick, P.M., Patuzzi, R., Robertson, D.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01-02-2004; Elsevier
• Subjects: Action Potentials - drug effects; Animals; Biological and medical sciences; Calcium channel; Calcium Channel Blockers - pharmacology; Calcium Channels, L-Type - drug effects; Calcium Channels, L-Type - physiology; Cochlea; Cochlea - drug effects; Cochlea - physiology; Compound action potential; Dose-Response Relationship, Drug; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation; Evoked Potentials, Auditory - drug effects; Female; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Hair Cells, Auditory - drug effects; Hair Cells, Auditory - secretion; Male; Neural noise; Neurotransmitter Agents - secretion; Nimodipine; Nimodipine - pharmacology; Transmitter; Vertebrates: nervous system and sense organs; SNN, spectrum of the spontaneous neural noise; Transmitter; Compound action potential; Neural noise; Calcium channel; N 1, first negative peak of CAP; SP, summating potential; DC, direct current; DMSO, dimethylsulfoxide; CAP, compound action potential; Nimodipine; Cochlea; P 1, first positive peak of CAP; N 2, second negative peak of CAP; Agonist; Calcium; Noise; Calcium antagonist; Action potential; Glutamate receptor; Ionic channel; Inner ear; Organ of hearing; Kainate receptor; Guinea pig; Dihydropyridine derivatives; Rodentia; Sound; Vertebrata; Mammalia; Evoked potential; Inner hair cell; Neurotransmitter; L-type calcium channel; Kainic acid
• ISSN: 0378-5955; 1878-5891
• DOI: 10.1016/S0378-5955(03)00374-5

The effects of the L-type Ca
2+ channel blocker nimodipine on the spectrum of the spontaneous neural noise (SNN) and the waveform of the gross sound-evoked compound action potential (CAP) were investigated by perilymphatic perfusion in the guinea pig cochlea. Both the SNN and the CAP were reversibly suppressed by nimodipine. The percentage reduction in SNN was dose-dependent in a manner very similar to the results obtained with the measures of CAP threshold changes. The reduction in the peak SNN caused by 10 μM nimodipine was the same as that caused by 500 μM kainic acid, which totally eliminated any neural responses. For 1 μM nimodipine there was an apparent dissociation between the SNN and CAP changes such that the SNN could be markedly suppressed with only very small changes in CAP thresholds. These results imply that spontaneous release of neurotransmitter from the inner hair cell is more sensitive to block of calcium channels than evoked release. There was no evidence for any marked shift caused by nimodipine, in the position of the main (900 Hz) spectral peak in the SNN. Comparison of the CAP waveform before and after nimodipine perfusion showed that the CAP waveforms were unchanged despite the change in sensitivity. These data do not support the notion of any significant postsynaptic site of action of nimodipine. The data hence provide further support for an exclusively presynaptic role for L-type Ca
2+ channels in the regulation of both evoked and spontaneous neurotransmitter release from inner hair cells.