Abstract
BackgroundCalcium sparks are ryanodine receptor mediated transient calcium signals that have been shown to hyperpolarize the membrane potential by activating large conductance calcium activated potassium (BK) channels in vascular smooth muscle cells. Along with voltage-dependent calcium channels, they form a signaling unit that has a vasodilatory influence on vascular diameter and regulation of myogenic tone. The existence and role of calcium sparks has hitherto been unexplored in the spiral modiolar artery, the end artery that controls blood flow to the cochlea. The goal of the present study was to determine the presence and properties of calcium sparks in the intact gerbil spiral modiolar artery.ResultsCalcium sparks were recorded from smooth muscle cells of intact arteries loaded with fluo-4 AM. Calcium sparks occurred with a frequency of 2.6 Hz, a rise time of 17 ms and a time to half-decay of 20 ms. Ryanodine reduced spark frequency within 3 min from 2.6 to 0.6 Hz. Caffeine (1 mM) increased spark frequency from 2.3 to 3.3 Hz and prolonged rise and half-decay times from 17 to 19 ms and from 20 to 23 ms, respectively. Elevation of potassium (3.6 to 37.5 mM), presumably via depolarization, increased spark frequency from 2.4 to 3.2 Hz. Neither ryanodine nor depolarization changed rise or decay times.ConclusionsThis is the first characterization of calcium sparks in smooth muscle cells of the spiral modiolar artery. The results suggest that calcium sparks may regulate the diameter of the spiral modiolar artery and cochlear blood flow.
Highlights
Calcium sparks are ryanodine receptor mediated transient calcium signals that have been shown to hyperpolarize the membrane potential by activating large conductance calcium activated potassium (BK) channels in vascular smooth muscle cells
We demonstrate for the first time, a detailed analysis of the kinetics and properties of Ca2+ sparks in smooth muscle cells of the intact gerbil spiral modiolar artery (SMA) and their regulation by pharmacological activators and inhibitors of ryanodine receptor (RyR) as well as changes in smooth muscle membrane potential
Staining with 1 μM Bodipy® FL-X ryanodine produced a pattern that was consistent with RyRs being uniformly expressed in the sarcoplasmic reticulum (Figure 1)
Summary
Calcium sparks are ryanodine receptor mediated transient calcium signals that have been shown to hyperpolarize the membrane potential by activating large conductance calcium activated potassium (BK) channels in vascular smooth muscle cells. The gerbil spiral modiolar artery (SMA) originates via the anterior inferior cerebellar artery from the basilar artery and provides the blood supply to the cochlea. It has an outer diameter of ~60 μm and follows the eighth cranial nerve from the brain stem to the modiolus of the cochlea [1]. The SMA is an end-artery that feeds the capillary networks of the spiral ligament and the stria vascularis, which maintains the endocochlear potential essential for hearing [2] This energy-intensive mechanism renders the cochlea vulnerable to ischemia, which is thought to be involved in the pathogenesis of hearing loss and tinnitus. The mechanisms that regulate the diameter of the SMA and thereby cochlear blood flow are of great interest.
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