The menthol receptor, Transient Receptor Potential Melastatin member 8 (TRPM8), is the principal sensor of cold in primary sensory neurones (Bautista et al., 2007). However, recently it has been described as a prominent vascular TRPM protein (Inoue et al., 2006, Yang et al., 2006). Previously we have shown that TRPM8 mRNA is expressed in a number of rat arteries including aorta, ventral tail, mesenteric and femoral artery (Melanaphy et al., 2008). In aortic, pulmonary and tail arterial smooth muscle TRPM8 activation increases cytosolic [Ca²⁺] and triggers myocyte contraction (Yang et al., 2006; Borisova et al., 2008). However, the localisation of the TRPM8 protein in vascular myocytes and the electrophysiological characteristics of its activation remain unknown. Ventral tail artery was obtained from humanely-dispatched Sprague-Dawley rats (12 weeks). Single vascular myocytes were then isolated by enzymatic digestion for immunocytochemistry and patch clamp analysis. Staining of isolated rat tail artery myocytes with TRPM8 rabbit antibody revealed TRPM8 immunoreactivity predominantly localised on the cells perimeter. In voltage-clamped tail artery myocytes, held at -20 to -40 mV, 300 μM menthol accelerated STOCs discharge from 2.8±0.4 s^-1 to 6.3±0.4 s^-1 (mean ± S.E.M.; paired t-test, P<0.01; N=4 (N = no. of cells)) and often resulted in a transient increase in whole cell current. In perforated patch clamp configuration, 300 μM menthol depolarised tail artery myocytes from a mean membrane potential of -56.8±3 mV by 8.3±1 mV (paired t-test, P<0.001; N=7). Most interestingly, menthol simultaneously increased the frequency of spontaneous hyperpolarisations from a mean of 0.3±0.1 s^-1 to 1.4±0.4 s^-1 (paired t-test, P<0.05; N=6). These hyperpolarisations also increased in amplitude from a mean of -11.8±3 mV to -22.8±3 mV (unpaired t-test, P<0.05; N=1, n=7-10 (n = no. of observations)). There were no other changes observed in the characteristics of the hyperpolarisations, e.g. time-to-peak and decay time constant. Taken together these findings suggest that TRPM8 activation causes acceleration of elementary Ca²⁺ store release events (sparks), resulting in increased BK_Ca channel activity. We conclude that the calcium permeable cation channel, TRPM8, is located on the periphery of tail artery vascular myocytes, and TRPM8 activation increases [Ca²⁺]_i resulting in increased BK_Ca channel activity. TRPM8 activation produces two distinct patterns of electrical activity, (i) sustained membrane depolarisation due to cation influx, and (ii) brief spontaneous hyperpolarisations of increased size and frequency due to TRPM8/Ca²⁺ sparks/BK_Ca channel coupling.