Neurobehavioral alterations plus transcriptional changes of the heat shock protein 90 and hypoxia inducible factor-1α in the crucian carp exposed to copper

The various physiological alterations caused by copper (Cu) exposure in fish have attracted great interests toward neuronal strategies against Cu toxicity. Here, neurobehavioral activities (including anxiety-like behaviors) and transcriptional levels of heat shock protein (Hsp)90 and hypoxia inducible factor-1alpha (HIF-1α) were evaluated in the crucian carp (Carassius carassius) treated with nominal sub-lethal higher (1.45 mg/L) and lower (0.30 mg/L) concentrations of CuCl2. Both concentrations accounted for diminished swimming speed and food intake plus a strong preference for the dark side of the light/dark apparatus together with a reduction of crossings between the two compartments with respect to controls. Contextually, Hsp90 and HIF-1α transcripts were largely down- and up-regulated, respectively, in some brain areas such as in the medial part of the dorsal telencephalon (Dm, −52%) and in the ventral part of the ventral telencephalon (Vv, +68%). When carps were transferred to CuCl2-free water, some behaviors were rescued especially for fish previously exposed to 0.30 mg/L concentration. In this same condition, Hsp90 mRNA levels were recuperated (−94%) in the medial preglomerular nucleus (NPGm) with respect to exposed fish while HIF-1α mRNA was mostly down-regulated in telencephalic stations. Moreover, recovery capacities of this extraordinary resistant fish was exhibited by evident reductions (−80%) of the dark argyrophilic granules such as in the ventral telencephalon (VTel). Overall, our results point to interesting responses against Cu toxicity involving Hsp90 and HIF-1α transcripts that may constitute early indicators of environmental stressors leading to the repair of metal-induced damages in fish with notable brain plasticity properties.