Background and Objectives : Auditory signal can be amplified by the organ of Corti and be detected in the auditory cortex. Outer hair cells (OHCs) play a pivotal role in this amplification process. The signal transduction mechanism of OHC relys
on
the
precise control of intracellular calcium ([Ca2+]i). Membrane depolarization, induced by electrical stimulation or extracellular high concentration of KCl solution, increases [Ca2+]i through the opening of voltage-gated
Ca2+ channel or the release from intracellular Ca2+ store which is stimulated by second messenger system. Efferent stimulation seems to inhibit the electromotility of OHC and modify the amplification process. Acetylcholine
is
the
most promising neurotransmitter released from efferent synapse. In this study, we aimed to observe the effect of carbamylcholine (a non-hydrolyzable, non-selective cholinergic agonist) on the change of [Ca2+]i, and the modification of
depolarization-induced [Ca2+]i increase in isolated OHCs of the guinea pig cochlea using the fluorescent indicator fluo-3. Materials and Method : Outer hair cells were isolated from the guinea pig cochlea and incubated in HBSS
containing
5 M
fluo-3 for 30 min. The [Ca2+]i was measured under inverted microscope equipped with epifluorescence system. The images were analysed and [Ca2+]i was calculated using Fmax, Fmin and Kd obtained from in vivo and in vitro
calibration.
Results : [Ca2+]i increased by extracellular carbamylcholine application (1mM) in OHCs. KCl solution could induce [Ca2+]i increase when used more than 25mM and the responses were concentration-dependent. Preincubation of
carbamylcholine, however, did not modify the depolarization-induced [Ca2+]i increase. Conclusion : Through these results, we speculate that the acetylcholine, released from the efferent synapse, can induce local increase of
[Ca2+]i, but acetylcholine can not regulate the depolarization-induced [Ca2+]i in isolated OHCs of the guinea pig cochlea.
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