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

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Abstract
We measured Ca2+ concentration, [Ca2+], transients in mitral cell distal apical dendritic tufts produced by physiological odour stimulation of the olfactory epithelium and electrical stimulation of the olfactory nerve (ON) using two‐photon scanning and conventional wide‐field microscopy of Ca2+‐Green‐1 dextran in an in vitro frog nose–brain preparation. Weak or strong ON shock‐evoked fluorescence transients always had short latency with an onset 0–10 ms after the onset of the bulb local field potential, rapidly increasing to a peak of up to 25% fractional fluorescence change (ΔF/F) in 10–30 ms, were blocked by 10 µm CNQX, decaying with a time constant of about 1 s. With stronger ON shocks that activated many receptor axons, an additional, delayed, sustained AP5‐sensitive component (peak at ≈ 0.5 s, up to 40% ΔF/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, regardless of the strength of the odour or the amplitude of the response. These were considerably larger (up to 150% ΔF/F) than those evoked by ON shock. Odour‐evoked [Ca2+] transients were also distinguished from ON shock‐evoked transients by tufts in different glomeruli responding with different delays (time to onset differed by up to 1.5 s between different tufts for the same odour). Odour‐evoked [Ca2+] transients were increased by AMPA‐kainate receptor blockade, but substantially blocked by AP5. Electrical stimulation of the lateral olfactory tract (5–6 stimuli at 10 Hz) that evoked granule cell feedback inhibition, blocked 60–100% of the odour‐evoked [Ca2+] transient in tufts when delivered within about 0.5 s of the odour. LOT‐mediated inhibition was blocked by 10 µm bicuculline.