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Impact of acute cadmium exposure on the trunk lateral line neuromasts and consequences on the “C-start” response behaviour of the sea bass (Dicentrarchus labrax L.; Teleostei, Moronidae)
Faucher, K.; Fichet, D.; Miramand, P.; Lagardère, J.-P. (2006). Impact of acute cadmium exposure on the trunk lateral line neuromasts and consequences on the “C-start” response behaviour of the sea bass (Dicentrarchus labrax L.; Teleostei, Moronidae). Aquat. Toxicol. 76(3-4): 278-294. https://dx.doi.org/10.1016/j.aquatox.2005.10.004
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X; e-ISSN 1879-1514, more
Peer reviewed article  

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Keywords
    Anatomical structures > Body organs > Animal organs > Sense organs > Lateral line
    Aquatic organisms > Marine organisms > Fish > Marine fish
    Chemical elements > Metals > Heavy metals > Cadmium
    Pollution effects
    Dicentrarchus labrax (Linnaeus, 1758) [WoRMS]; Moronidae Jordan & Evermann, 1896 [WoRMS]
    Marine/Coastal
Author keywords
    fish; sea bass; lateral line system; neuromast; acute cadmium exposure;C-start; escape behaviour

Authors  Top 
  • Faucher, K.
  • Fichet, D.
  • Miramand, P.
  • Lagardère, J.-P., more

Abstract
    Behavioural responses of sea bass Dicentrarchus labrax were investigated after exposure to cadmium ions in laboratory-controlled conditions. The aim of this study was to discover whether environmental exposure to cadmium ions inactivates fish lateral line system neuromasts, and to determine the behavioural consequences of such a sensory blockage. For this, fish escape behaviour in response to an artificial water jet was recorded using a 25-frames s-1 analog video camera before and after cadmium exposure. Experimental set up was tested with fish whose lateral line system was artificially inactivated by antibiotics (gentamicin and streptomycin). Histological analyses with scanning electron microscopy showed antibiotic treatment destroyed lateral line system neuromasts. In addition, these fish did not respond to stimulations provoked by the water jet after antibiotic treatment. Fish escape behaviour was then recorded before and after cadmium exposure at two different concentrations. When fish were exposed to the first concentration of cadmium tested (0.5 µg l-1, which represents the maximal cadmium concentration encountered in contaminated estuaries), no alteration in neuromast tissue was observed. In addition, before cadmium exposure, fish responded positively in 98.41 ± 4.95% of lateral line system stimulations (escape behaviour in response to the water jet). After cadmium exposure, no behavioural modification could be detected: the fish responded positively in 95.16 ± 9.79% of stimulations (?2 = 2.464, p = 0.116). In contrast, the high cadmium concentration used (5 µg l-1, which represents 10 times the concentration occurring in highly polluted estuarine areas) involved severe neuromast tissue damage. Just after such cadmium exposure, fish showed only 41.67 ± 35.36% of positive responses to their lateral line system stimulations, while they responded positively in 95.93 ± 9.10% of stimulations under control conditions (?2 = 24.562, p < 0.0001). Their lateral line system neuromasts seemed to regenerate about 1 month after cadmium exposure. Associated with this regeneration, from the 21st day after cadmium exposure, their escape behaviour had recovered and was not significantly different from that recorded under control conditions (86.74 ± 20.82%, ?2 = 2.876, p = 0.090). This study shows that although 5 µg l-1 cadmium is able to damage lateral line system neuromasts and causes fish behavioural alterations, fish exposed to 0.5 µg l-1 cadmium displayed neither tissue neuromast nor behavioural modification.

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