FIGURE 9

Brain of D. rerio submitted to low temperatures show high levels of the aanat2 transcripts causing a putative increase in melatonin synthesis. We suggested that expression of melatonin receptors (mtnr1aa and mtnr1bb) may decrease to ensure homeostasis. In turn, it is known that mtnr1aa, mtnr1bb (Gi protein-coupled receptors) inhibit adenylate cyclase activity which ultimately leads to the inhibition of CREB phosphorylation, a transcription factor required for clock gene expression, resulting in a reduction of their transcripts. Also, in the brain we found a reduction in the gh1 transcripts at lower temperature, leading to a decrease of ghra and ghrb in the muscle, and igf1ra, igf1rb in the liver, suggesting a long-term inhibition of the animal growth. In turn, clock genes are capable to bind to the promoter E-box region of genes as gh1 thus modulating its expression (a putative inhibition in our study). On the other hand, there was an increase in the cortisol concentration and a compensatory reduction of its receptor transcripts. The glucocorticoid (Gc)/glucocorticoid receptor complex modulates the expression of clock genes by binding to glucocorticoid response elements (GRE) in their promoters. Consequently, we evidenced a decrease in the expression of clock genes in all organs analyzed. This may be associated to cold-modulation by melatonin and cortisol pathways or a direct effect of low temperature on clock gene transcripts.