Animal agonistic behaviors, including threat, combat, submission and chase, are complex responses to experimental stimuli. Animal behaviors are regulated by the central nervous system. In the central nervous system, the biogenic amine serotonin has been thought to serve important roles in animal aggression (including fish), but it¡¦s not clear if serotonin affects threatening and fighting differently. This study took experimental approaches to examine the effects of this neurotransmitter on threatening and fighting in a paradise-fish model in which the complex agonistic behavior is well characterized. Treatments with serotonin synthesis precursor tryptophan (0.125mg/g) to one of the two contestants had insignificant effects on threatening or fighting while synthesis blocker p-Chlorophenylalanine (PCPA) (0.3mg/g) decreased threatening time and occurrences of head-tail display. When these drugs were added to both contestants, tryptophan reduced all agonistic behavioral patterns displays, and PCPA decreased threatening time and head-tail display. In addition to changes in behavioral patterns, tryptophan led the fish to be attacked. In contrast, PCPA led the injected fish to actively attack its opponent. However, tryptophan and PCPA had no effect on social status in parasise fish. I suggest that agonistic responses and the initial fighting decision in a paradise fish are affected not only by level of its serotonin, but also by the behavioral responses of its opponent. And the establishment of outcome of encounter is affected more by the environmental stimuli than the serotonin level.

In this study, p-chlorophenylalanine (pCPA), an inhibitor of tryptophan hydroxylase (the rate limiting enzyme of serotonin synthesis), was used to reduce serotonin (5HT) levels during early development in zebrafish embryos. One day old dechorionated embryos were treated with 25μM pCPA for 24h and subsequently rescued. Immunohistological studies using a 5HT antibody confirmed that 5HT neurons in the brain and spinal cord were depleted of transmitter by 2days post fertilization (dpf). Twenty four hours after pCPA exposure embryos were unable to burst swim and were nearly paralyzed. Movement began to improve at 4dpf, and by 7dpf, larvae exhibited swimming activity. Rescued larvae continued to grow in rostrocaudal length over 5days post-rescue, but their length was always 16-21% below controls. Surprisingly, both groups displayed the same number of myotomes. To examine whether hypertonicity of myotomes in treated embryos played a role in their shorter rostrocaudal lengths, 1dpf embryos were exposed to a combination of 25μM pCPA and 0.6mM of the sodium channel blocker ethyl 3-aminobenzoate methanesulfonate (MS-222). After a 24hour exposure, the embryos exhibited the same rostrocaudal length as control embryos suggesting that myotome hypertonicity plays a major role in the decreased axial length of the treated larvae. In addition, pCPA treated 2dpf embryos exhibited abnormal notochordal morphology that persisted throughout recovery. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to determine the relative levels of the serotonin 1A receptor (5HT 1A) transcript and the serotonin transporter (SERT) transcript in the brain and spinal cord of control and treated embryos. Transcripts were present in both brain and spinal cord as early as 1dpf and reached maximal concentrations by 3dpf. Embryos treated with pCPA demonstrated a decrease in the concentration of 5HT 1A transcript in both brain and spinal cord. While SERT transcript levels remained unaffected in brain, they were decreased in spinal cord. Five days subsequent to pCPA rescue, 5HT 1A transcript concentrations remained decreased in brain while SERT transcript levels were elevated in both regions. These findings suggest that reduction of 5HT during early zebrafish development may have an adverse effect on body length, notochordal morphology, locomotor behavior, and serotonin message-related expression.

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