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M.M. Lecchi, S. Picaud, A.B. Safran, D. Bertrand; Chronic Nicotine Treatment and Retinal Development . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3948.
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Tobacco smoking during pregnancy has been associated with foetus anomalies thought to be mediated by the activation of neuronal nicotinic acetylcholine receptors. As this family of receptors is widely expressed in the central nervous system at developmental stages, preceding synapse formation, it can be postulated that nicotine absorbed by the mother can bind in the foetus on these ligand–gated channels. Moreover, it was shown that chronic nicotine exposure causes an increase in ligand binding in non–smokers versus smokers’ brain. Nicotinic acetylcholine receptors are also expressed in the vertebrate retina and it was shown that they contribute to calcium wave activity during development. Purpose: In view of the importance of neuronal nicotinic acetylcholine receptors both in development and adulthood we investigated the effect of chronic nicotine exposure during embryogenesis. Methods: Effects of exposure of chick embryos to nicotine concentrations found in the plasma of smokers were analyzed both at the morphological and physiological levels. Patch–clamp recordings of ganglion cells were used to monitor the responses evoked by acetylcholine and specific agonists or antagonists. Classification of neuronal nicotinic acetylcholine receptor subtypes was done according to their physiological and pharmacological signatures. Results: Results obtained from a large number of cells show for the first time that functional neuronal nicotinic acetylcholine receptors can be investigated as early as E12 and that they progressively evolve as neurons are maturating. Chronic nicotine exposure (100 nM to 1 µM) causes significant modifications in the number of acetylcholine responsive cells that can be observed at E17–18. Conclusions: Taken together these data illustrate the importance of nicotinic receptors during retinal development.
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