Calcium sparks in the intact gerbil spiral modiolar artery

Calcium 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.This 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.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. Consequently, the mechanisms that regulate the diameter of the SMA and thereby cochlear blood flow are of great interest.Vascular tone is determined by the contractility of the smooth muscle cell, which is regulated by membrane-potential and Ca2+-dependent as well as independent mechanisms [3]. An important regulator of smooth muscle contractility is the ryanodine receptor (RyR) mediated "Ca2+ spark". Ca2+ sparks are the physical manifestation of coordinated openings of clustered RyRs causing a highly localized and transient incre