Odour-evoked [Ca2+] transients in mitral cell dendrites of frog olfactory glomeruli

We measured Ca2+ concentration, [Ca2+], transients in mitral cell distal ap ical dendritic tufts produced by physiological odour stimulation of the olf actory epithelium and electrical stimulation of the olfactory nerve (ON) us ing two-photon scanning and conventional wide-field microscopy of Ca2+-Gree n-1 dextran in an in vitro frog nose-brain preparation. Weak or strong ON s hock-evoked fluorescence transients always had short latency with an onset 0-10 ms after the onset of the bulb local field potential, rapidly increasi ng to a peak of up to 25% fractional fluorescence change (DeltaF/F) in 10-3 0 ms, were blocked by 10 mum CNQX, decaying with a time constant of about 1 s. With stronger ON shocks that activated many receptor axons, an addition al, delayed, sustained AP5-sensitive component (peak at approximate to 0.5 s, up to 40% DeltaF/F maximum) could usually be produced. Odour-evoked [Ca2 +] transients sometimes displayed a rapid onset phase that peaked within 50 ms but always had a sustained phase that peaked 0.5-1.5 s after onset, reg ardless of the strength of the odour or the amplitude of the response. Thes e were considerably larger (up to 150% DeltaF/F) than those evoked by ON sh ock. Odour-evoked [Ca2+] transients were also distinguished from ON shock-e voked transients by tufts in different glomeruli responding with different delays (time to onset differed by up to 1.5 s between different tufts for t he same odour). Odour-evoked [Ca2+] transients were increased by AMPA-kaina te receptor blockade, but substantially blocked by AP5. Electrical stimulat ion of the lateral olfactory tract (5-6 stimuli at 10 Hz) that evoked granu le cell feedback inhibition, blocked 60-100% of the odour-evoked [Ca2+] tra nsient in tufts when delivered within about 0.5 s of the odour. LOT-mediate d inhibition was blocked by 10 mum bicuculline.