Effects of nicotine on odor-induced increases in regional blood flow in the olfactory bulb in rats
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The present study examined the effects of nicotinic acetylcholine receptor activation on the odor-induced blood flow response in the olfactory bulb. In urethane-anesthetized rats, odor stimulation (5% amyl acetate, 30 s) produced an increase in olfactory bulb blood flow (reaching 107% ± 3% of the pre-stimulus basal values), without changes in frontal cortical blood flow or mean arterial pressure. Intravenous injection of nicotine (30 μg/kg), a nicotinic acetylcholine receptor agonist, significantly augmented the odor-induced increase response of olfactory bulb blood flow, without changes in the basal blood flow level. The nicotine-induced augmentation of the olfactory bulb blood flow response to odor was negated by dihydro-β-erythroidine, an α4β2-preferring nicotinic acetylcholine receptor antagonist. Our results suggest that the activation of α4β2-like neuronal nicotinic acetylcholine receptors in the brain potentiates an odor-induced blood flow response in the olfactory bulb.
KeywordsOlfactory bulb Nicotinic acetylcholine receptor Regional cerebral blood flow Odor stimulation Rat
SU and FK conceived and designed the research; all the authors performed experiments, analyzed data, and interpreted the results of the experiments; SU drafted the manuscript; SU and FK edited and revised the manuscript; and all the authors approved the final manuscript.
This work was supported by JSPS KAKENHI (Grant number 15K08225 to SU) and by the Smoking Research Foundation.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflicts of interest.
All applicable international, national, and/or institutional guidelines for the care and use of animals were followed. This article does not contain any studies performed by any of the authors with human participants.
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