Losses of immunoreactive parvalbumin amacrine and immunoreactive αprotein kinase C bipolar cells caused by methylmercury chloride intoxication in the retina of the tropical fish Hoplias malabaricus

To quantify the effects of methylmercury (MeHg) on amacrine and on ON-bipolar cells in the retina, experiments were performed in MeHgexposed groups of adult trahiras (Hoplias malabaricus) at two dose levels (2 and 6 μg/g, ip). The retinas of test and control groups were processed by mouse anti-parvalbumin and rabbit anti-αprotein kinase C (αPKC) immunocytochemistry. Morphology and soma location in the inner nuclear layer were used to identify immunoreactive parvalbumin (PV-IR) and αPKC (αPKC-IR) in wholemount preparations. Cell density, topography and isodensity maps were estimated using confocal images. PV-IR was detected in amacrine cells in the inner nuclear layer and in displaced amacrine cells from the ganglion cell layer, and αPKC-IR was detected in ON-bipolar cells. The MeHgtreated group (6 μg/g) showed significant reduction of the ON-bipolar αPKC-IR cell density (mean density = 1306 ± 393 cells/mm2) compared to control (1886 ± 892 cells/mm2; P < 0.001). The mean densities found for amacrine PV-IR cells in MeHg-treated retinas were 1040 ± 56 cells/mm2 (2 μg/g) and 845 ± 82 cells/mm2 (6 μg/g), also lower than control (1312 ± 31 cells/mm2; P < 0.05), differently from the data observed in displaced PV-IR amacrine cells. These results show that MeHg changed the PV-IR amacrine cell density in a dose-dependent way, and reduced the density of αPKC-IR bipolar cells at the dose of 6 μg/g. Further studies are needed to identify the physiological impact of these findings on visual function. Correspondence