In two experiments, a computerized on-demand feeding system coupled with a PIT tag monitoring device was used to continuously record the triggering activity by ca. 50 individual sea bass for 55 days (Exp. 1, initial average body weight and coefficient of variation, CV: 299 g, 15%) and 69 days (Exp. 2, 157 g, 13%). Each group was stocked in 1 m3 tanks and exposed to a water temperature of 21 ± 1 °C and a light regime of 16:8 LD. Only 5% of the triggering activity was not associated with simultaneous PIT tag detection. Although each individual was detected via PIT tag during the experiment, only 67% and 74% of the fish actuated the trigger at least once in Exp. 1 and Exp. 2, respectively. Moreover, only two fish in Exp. 1 and one fish in Exp. 2 accounted for 82% (43 + 39) and 77% of the total triggering activity, respectively. These three, high-triggering individuals did not exhibit a higher specific growth rate or agonistic behavior as observed by video monitoring. Indeed, zero-triggering fish had either a slightly higher SGR (Exp. 1) or a higher final body weight (Exp. 2) compared with low-and high-triggering fish.

In Teleost fish, development, growth, and reproduction are influenced by the daily and seasonal variations of photoperiod and temperature. Early in vivo studies indicated the pineal gland mediates the effects of these external factors, most probably through the rhythmic production of melatonin. The present investigation was aimed at determining whether melatonin acts directly on the pituitary to control GH and prolactin (PRL) secretion in rainbow trout. We show that 2-[125I]-iodomelatonin, a melatonin analog, binds selectively to membrane preparations and tissue sections from trout pituitaries. The affinity was within the range of that found for the binding to brain microsomal preparations, but the number of binding sites was 20-fold less than in the brain. In culture, melatonin inhibited pituitary cAMP accumulation induced by forskolin, the adenyl cyclase stimulator. Forskolin also induced an increase in GH release, which was reduced in the presence of picomolar concentrations of melatonin. At higher concentrations, the effects of melatonin became stimulatory. In the absence of forskolin, melatonin induced a dose-dependent increase in GH release, and a dose-dependent decrease in PRL release. Melatonin effects were abolished upon addition of luzindole, a melatonin antagonist. Our results provide the first evidence that melatonin modulates GH and PRL secretion in Teleost fish pituitary. Melatonin effects on GH have never been reported in any vertebrate before. The effects result from a direct action of melatonin on pituitary cells. The complexity of the observed responses suggests several types of melatonin receptors might be involved.

The individual food-demand behavior of juvenile European sea bass (Dicentrarchus labrax, L.) reared in groups under self-feeding conditions was investigated. The triggering activity on self-feeder, i.e. index of the food-demand activity, agonistic interactions and territorial behavior were monitored for periods of 42 to 68 days in six groups of 50 fish. The specific growth rate was calculated and the brain serotonergic activity was used as a stable index of social stress. Inter-individual differences appeared in triggering activity and three groups were distinguished: 3-5 high-triggering fish, 17-30 low-triggering fish and the remaining individuals were null-triggering fish. There were no significant differences in specific growth rates calculated at the end of the experiment (day 42 or day 68) between individuals with high, low, and null food-demand (ANOVA, p>0.05). No territorial or agonistic behaviors were observed, however, there were significant differences in brain serotonergic activity between the three triggering groups (ANOVA, p=0.050 in telencephalon and p=0.004 in cerebellum). Specifically, high-triggering fish had lower serotonergic turnover than low or null-triggering fish. We put forth the hypothesis that fish with low or null-triggering activity could be stressed by the high activity of high-triggering individuals.

Objective. We have previously shown that interleukin-1␤ (IL-1␤) impairs transforming growth factor ␤ (TGF␤) signaling through TGF␤ receptor type II (TGF␤RII) down-regulation and Smad7 upregulation. This mechanism could account for the reduced responsiveness of osteoarthritic chondrocytes to TGF␤ and the cartilage breakdown linked to this disease. The aim of this study was to investigate the molecular mechanism underlying the IL-1␤-induced stimulation of Smad7 in human articular chondrocytes.Methods. Human articular chondrocytes were treated with IL-1␤ in the presence of TGF␤1, pyrrolidine dithiocarbamate (a repressor of the NF-B pathway), or cycloheximide. Then, steady-state messenger RNA and protein levels were estimated by real-time reverse transcription-polymerase chain reaction and immunocytology. In addition, transient transfections of p65 expression vector or p65-targeted short hairpin RNA were performed to define the effect of NF-B on Smad7 expression.Results. TGF␤RII overexpression restored the TGF␤ response of human articular chondrocytes. However, this effect was transient, implying that a secondary mechanism was responsible for the alteration of the TGF␤ response with long-term exposure to IL-1␤. Moreover, IL-1␤ caused a late induction of the inhibitory Smad7. This effect was direct, since it did not require de novo synthesis. In addition, we established, by experiments with gain/loss of function, that the up-regulation of Smad7 by IL-1␤ is mediated through the NF-B pathway, especially the p65 subunit.Conclusion. These findings clarify the regulatory process of IL-1␤ on Smad7 expression. Understanding the molecular basis of IL-1␤ induction of Smad7 and the reduction of chondrocyte responsiveness to TGF␤ provides new insights into the molecular mechanisms of osteoarthritis and may facilitate the identification of novel approaches for its treatment.

Acoustic communication allows the exchange of information within specific contexts and during specific behaviors. The blind, cave-adapted and the sighted, river-dwelling morphs of the species Astyanax mexicanus have evolved in markedly different environments. During their evolution in darkness, cavefish underwent a series of morphological, physiological and behavioral changes, allowing the study of adaptation to drastic environmental change. Here we discover that Astyanax is a sonic species, in the laboratory and in the wild, with sound production depending on the social contexts and the type of morph. We characterize one sound, the “Sharp Click”, as a visually-triggered sound produced by dominant surface fish during agonistic behaviors and as a chemosensory-, food odor-triggered sound produced by cavefish during foraging. Sharp Clicks also elicit different reactions in the two morphs in play-back experiments. Our results demonstrate that acoustic communication does exist and has evolved in cavefish, accompanying the evolution of its behaviors.