Intracerebroventricular administration of arginine vasotocin (AVT) induces anorexigenesis and anxiety-like behavior in goldfish.

Peptides

Laboratory of Regulatory Biology, Graduate School of Science and Engineering, University of Toyama, Toyama 930-8555, Japan; Laboratory of Regulatory Biology, Graduate School of Innovative Life Sciences, University of Toyama, Toyama 930-8555, Japan. Electronic address:

Published: September 2019

Arginine vasotocin (AVT) is known as a neurohypophyseal hormone that regulates water- and mineral-balance in non-mammalian vertebrates. Recent studies revealed that AVT also exerts central effects on behavior. The goldfish has several merits for evaluation of behavioral changes. However, there is few information on the behavioral action of AVT in this species. Here we examined the effects of AVT on food intake and psychomotor activity. AVT was administered intracerebroventricularly at 1, 5 and 10 pmol g body weight (BW). Intracerebroventricular (ICV) administration of AVT at 5 and 10 pmol g BW significantly decreased food intake during 30 min after injection and recovery from anesthesia. The AVT-induced anorexigenic action was attenuated by treatment with the AVT receptor V1aR antagonist Manning compound (MC) at 50 pmol g BW. As the goldfish tends to prefer the lower to the upper area of a tank, we used this preference behavior for assessing psychomotor activity during a 30-min observation period. ICV administration of AVT at 1, 5 and 10 pmol g BW significantly prolonged the time spent in the lower area, but did not affect locomotor activity in the tank at any dose. The action of AVT was similar to that of the central-type benzodiazepine receptor inverse agonist FG-7142 at 10 pmol g BW. AVT-induced anxiety-like behavior was blocked by treatment with MC at 50 pmol g BW. These results indicate that AVT affects food intake and psychophysiological status, and also induces anorexigenic- and anxiogenic-like actions via the V1aR-signaling pathway in the goldfish brain.

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http://dx.doi.org/10.1016/j.peptides.2019.170118DOI Listing

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