engleski

Effects of imidacloprid on F11 cellular model.

Neuronal excitability is a parameter related to neuron potential to generate signals of novel stimuli. Long-term exposure to environmental chemicals is believed to be a predisposing factor for further establishment of altered neuronal functions that often can be translated into chronic neuronal diseases. The molecular irreversible events leading chemical exposure to become risk factors for neuronal sensitisation, however are not yet completely understood. Imidacloprid is an insecticide of the neo-nicotinoid family, that operate preferentially via nicotinic neuronal receptors expressed on both invertebrates and mammalian cells. In this work, we explored the effects of imidacloprid (0.1 - 4 mM) on F11 neuronal cell cultures. At first we performed immunofluorescence to characterise expression of nicotinic ACh receptors in F11 cells, in control and after imidacloprid treatment. Cells were first than analysed for survival, total protein content and reactivity of enzymes involved in stress reactions. At low doses imidacloprid induced, as nicotine, higher extention of neurite processes and consequent stress-induced tubulin acetylation. Finally, imidacloprid exposure activates MAP kinase p38 and increase stability of Nrf2. Imidacloprid induced also reorganisation of a3 –containing nicotinic ACh receptors, an effect partly prevented by the antagonist mecamylamine (1mM, 1h). These results contribute to new assessment of imidacloprid effects on mammalian tissue.

F11 cells; neurons; neonicotinoids; imidacloprid

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