Cadmium exposure exerts neurotoxic effects in peacock blennies Salaria pavo

- Low amounts of Cd in the brain of peacock blennies despite a sublethal exposure to CdCl2.
- Selective permeability of the blood brain barrier.
- mRNA expression of two abc transporters significantly affected.
- Histopathological damages in the optic tectum and cerebellum.
- Cerebellum identified as the most sensitive organ to Cd.

Cadmium (Cd) is considered as an important factor involved in several neurological disturbances. The aim of this study was to assess the effects of Cd in the brain of peacock blennies Salaria pavo, a species used as a bioindicator of water pollution. A sublethal contamination of 2 mg CdCl2 L−1 was performed over periods of 1, 4, 10 and 15 days. Total Cd accumulation was measured in brains and displayed low concentrations throughout the experiment. Partial-length cDNA of different ATP-binding cassette transporters (abcb1, abcc1, abcc2, abcg2 proteins) and acetylcholinesterase (ache) were characterized. mRNA expressions profiles displayed an up-regulation of abcc2 mRNA after 4 days of Cd exposure only while abcg2 mRNA was down-regulated after 10 days only. For AChE, the mRNA transcription and the activity of the enzyme were followed and highlighted that Cd exerted an inhibitory effect on the nervous information transmission. At the histological level, fish exhibited pathological symptoms in the optic tectum and the cerebellum and results showed that the cerebellum was the most affected organ.