Rotenone alters behavior and reproductive functions of freshwater catfish, Mystus cavasius, through deficits of dopaminergic neurons in the brain.

Abstract

Rotenone, commonly used as a pesticide in agriculture and as a piscicide in aquaculture, is a toxic compound that causes dopaminergic neuronal cell loss in the substantia nigra pars compacta of the brain. At the neuroendocrine level, dopamine (DA) drives behavioral (locomotion, emotion, feeding, and social interactions, etc.) and reproductive functions of fish. In the current investigation, we examined effects of rotenone toxicity on neurobehavioral and reproductive functions in whole brain and in selected brain regions in an Indian freshwater catfish, locally known as gulsha (Mystus cavasius). After fish were exposed to water containing rotenone at 0, 2.5, 25, and 250\xa0μg/L for 2 days, significant reductions of DA, 3,4-dihydroxyphenylacetic acid (DOPAC; a DA metabolite), and their ratio (DOPAC/DA) were observed in whole brain at 250\xa0μg/L ambient concentrations of rotenone. When fish were treated with rotenone at 250\xa0μg/L concentration for 2 days, there was a significant reduction of DA, DOPAC and DOPAC/DA in diencephalon, DA and DOPAC in pituitary, and only DA in the telencephalon, compared with control fish. In parallel, numbers of tyrosine hydroxylase-positive (TH+) neurons declined significantly in the diencephalon and pituitary after rotenone treatment. Slowed, spontaneous movement and reduced feeding behavior were observed in rotenone-treated fish. Rotenone treatment resulted in a significantly higher gonadosomatic index with many mature vitellogenic oocytes in ovaries and lowered dopaminergic activity in these fish. These results indicate that rotenone influences neurobehavioral and reproductive functions through dopaminergic neuronal cell loss in gulsha brain.