T-type Ca2+ channels mediate propagation of odor-induced Ca2+ transients in rat olfactory receptor neurons

Propagation of odor-induced Ca2+ transients from the cilia/knob to the soma in mammalian olfactory receptor neurons (ORNs) is thought to be mediated exclusively by high-voltage-activated Ca2+ channels. However, using confocal Ca2+ imaging and immunocytochemistry we identified functional T-type Ca2+ channels in rat ORNs. Here we show that T-type Ca2+ channels in ORNs also mediate propagation of odor-induced Ca2+ transients from the knob to the soma. In the presence of the selective inhibitor of T-type Ca2+ channels mibefradil (10–15 μM) or Ni2+ (100 μM), odor- and forskolin/3-isobutyl-1-methyl-xanthine (IBMX)-induced Ca2+ transients in the soma and dendrite were either strongly inhibited or abolished. The percentage of inhibition of the Ca2+ transients in the knob, however, was 40–50% less than that in the soma. Ca2+ transients induced by 30 mM K+ were partially inhibited by mibefradil, but without a significant difference in the extent of inhibition between the knob and soma. Furthermore, an increase of as little as 2.5 mM in the extracellular K+ concentration (7.5 mM K+) was found to induce Ca2+ transients in ORNs, and such responses were completely inhibited by mibefradil or Ni2+. Total replacement of extracellular Na+ with N-methyl-d-glutamate inhibited none of the odor-, forskolin/IBMX- or 7.5 mM K+-induced Ca2+ transients. Positive immunoreactivity to the Cav3.1, Cav3.2 and Cav3.3 subunits of the T-type Ca2+ channel was observed throughout the soma, dendrite and knob. These data suggest that involvement of T-type Ca2+ channels in the propagation of odor-induced Ca2+ transients in ORNs may contribute to signal transduction and odor sensitivity.