Isolation increases milt production in goldfish

✍ Scribed by Fraser, E. Jane ;Stacey, Norm

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 191 KB
• Volume: 293
• Category: Article
• ISSN: 0022-104X
• DOI: 10.1002/jez.10120

✦ Synopsis

Abstract

Milt volume in goldfish is increased by female steroid and prostaglandin pheromones, by exposure to males with elevated gonadotropin levels, and by isolation from conspecifics. This study examined various aspects of the isolation effect on milt volume and serum gonadotropin II (GTH II). The latency of isolation‐induced milt increase in this study (12–24 hr) was longer than the latencies to pheromone‐induced milt increase in previous work (0.5–6.0 hr), was not affected by the time of day at which males were isolated, persisted for at least 72 hr in isolated males, and was terminated within 24 hr in males that were returned to groups. Isolated males maintained high milt production when separated from tank mates by a perforated barrier or when exposed to visual and odor cues from males in other tanks, suggesting that the unknown conspecific cues that maintain low milt production in groups operate at close range. Isolation appears to increase milt through a mechanism different from that mediating response to female pheromones because: (1) unlike female pheromones, which consistently increase serum GTH II, no isolation or regrouping treatment in this study affected male GTH II concentration; and (2) the effects of isolation and of exposure to the female pheromone 17α,20β‐dihydroxy‐4‐pregnen‐3‐one (17,20β‐P) are additive. Finally, males that were previously isolated or exposed to 17,20β‐P increased milt (but not GTH II) in grouped males, suggesting that the effects of isolation and pheromone exposure can indirectly stimulate male conspecifics. Although the biological function of the isolation effect is not clear, we propose that it illustrates the effect of removal from inhibitory cues normally received from male conspecifics. J. Exp. Zool. 293:511–524, 2002. © 2002 Wiley‐Liss, Inc.