Abstract

In this study, we determined whether the 201Tl (thallium-201)-based olfactory imaging is affected if olfactory sensory neurons received reduced pre-synaptic inhibition signals from dopaminergic interneurons in the olfactory bulb in vivo. The thallium-201 migration rate to the olfactory bulb and the number of action potentials of olfactory sensory neurons were assessed 3 h following left side nasal administration of rotenone, a mitochondrial respiratory chain complex I inhibitor that decreases the number of dopaminergic interneurons without damaging the olfactory sensory neurons in the olfactory bulb, in mice (6–7 animals per group). The migration rate of thallium-201 to the olfactory bulb was significantly increased following intranasal administration of thallium-201 and rotenone (10 μg rotenone, p = 0.0012; 20 μg rotenone, p = 0.0012), compared with that in control mice. The number of action potentials was significantly reduced in the olfactory sensory neurons in the rotenone treated side of 20 μg rotenone-treated mice, compared with that in control mice (p = 0.0029). The migration rate of thallium-201 to the olfactory bulb assessed with SPECT-CT was significantly increased in rats 24 h after the left intranasal administration of thallium-201 and 100 μg rotenone, compared with that in control rats (p = 0.008, 5 rats per group). Our results suggest that thallium-201 migration to the olfactory bulb is increased in intact olfactory sensory neurons with reduced pre-synaptic inhibition from dopaminergic interneurons in olfactory bulb glomeruli.

Highlights

  • Detecting the mechanisms underpinning olfactory dysfunction is challenging, owing to the difficulty in directly viewing the connectivity of peripheral olfactory nerves using current magnetic resonance imaging (MRI)

  • The thallium-201 migration rate to the olfactory bulb, as assessed with SPECT-CT, was significantly increased in normal rats 24 h following intranasal administration of 201Tl and 100 μg rotenone, compared with the rate following treatment with 201Tl and vehicle control (1% DMSO in phosphate-buffered saline (PBS)) (Fig. 5a, Mann-Whitney test, p = 0.008, 5 rats per group)

  • We aimed to determine whether thallium-201 migration to the olfactory bulb is affected by pre-synaptic inhibition of olfactory sensory neurons from the dopaminergic interneurons in the olfactory bulb in vivo

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Summary

Introduction

Detecting the mechanisms underpinning olfactory dysfunction is challenging, owing to the difficulty in directly viewing the connectivity of peripheral olfactory nerves using current magnetic resonance imaging (MRI). Thallium-201-based olfactory imaging is referred to as olfactory scintigraphy. The radioisotope thallium-201 is transported within olfactory neural tracts after nasal administration in rodents [3]. This transport is significantly decreased by transecting olfactory nerve fibers and correlates with odor detection ability in mice [4, 5]. Thallium can readily substitute potassium at the sodium/potassium (Na+/K+)-membrane adenosine triphosphatase (ATPase) activation sites [6]. Nasally administered thallium-201 may be transported into olfactory nerve cells as a substitute for potassium

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