title: Functional evidence for calcium-induced calcium release in isolated rat vibrissal Merkel cell mechanoreceptors.
abstract: 1. Single unit recordings were made from Merkel cell (sinus hair type I; St I) and sinus hair type II (St II) mechanoreceptors in isolated rat vibrissae. Responses were determined as the number of spikes evoked by controlled mechanical displacement of the hair shaft for 5 s every 30 s. 2. Superfusion of caffeine (10 mM) increased the responses of Merkel cell receptors by 50-180% of control (mean +/- S.E.M., 64 +/- 12.6%, n = 6, P < 0.001). Similar concentrations of caffeine inhibited St II receptor responses by 20-60% (mean +/- S.E.M., 35 +/- 8%, n = 5, P < 0.01). In both receptor types, caffeine induced a low-frequency increase in spontaneous firing. 3. When Merkel cell receptor responses were completely blocked by superfusion of high Mg2+-containing solution (to competitively block Ca2+ influx) caffeine had no effect when added after complete inhibition, but when added during partial inhibition of responses, the Mg2+-induced inhibition was transiently reversed or halted. This suggests that Ca2+ influx was a prerequisite for the action of caffeine. 4. Ryanodine (1 microM) increased the responses of Merkel cell receptors to mechanical stimulation by 7-60% (mean +/- S.E.M., 32 +/- 10.9 %, n = 5, P < 0.05) but had no effect on St II receptor responses. 5. The Ca2+-induced Ca2+ release (CICR) inhibitor procaine inhibited St I receptor responses in a concentration-dependent manner. Near-maximal inhibition was attained with 100 microM procaine. In four St I units, mean responses were depressed to 25% of control values. When both procaine (100 microM) and caffeine (10 mM) were introduced together, no net effect was seen. The responses of St II receptors were little affected by up to 100 microM procaine superfusion. 6. It is concluded that the mechano-electrical transduction process in St I receptors (but not St II) includes a CICR pathway. Taken with previous findings on the role of Merkel cells, it is likely that CICR is occurring in the Merkel cells.
authors.affiliation: Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin. senok1928@cuhk.edu.hk
authors.forename: S S
authors.initials: SS
authors.lastname: Senok
authors.forename: K I
authors.initials: KI
authors.lastname: Baumann
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D004594:Electrophysiology / Q000379:methods; D066298:In Vitro Techniques; D007700:Kinetics; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D018862:Merkel Cells / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D010812:Physical Stimulation; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012433:Ryanodine / Q000494:pharmacology; D015398:Signal Transduction; D013997:Time Factors; D014738:Vibrissae / Q000294:innervation*
chemical_list: D012433:Ryanodine; D002110:Caffeine; D011343:Procaine; D008274:Magnesium; D002118:Calcium