Philippe Levesque

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The interaction of methyl mercury (MeHg) with nerve-terminal mitochondria as a potential mechanism for its effects on the release of acetylcholine (ACh) was studied using rat brain synaptosomes. The primary goal was to assess the relative contribution of extracellular Ca2+ and Ca2+ released from nerve-terminal mitochondria to the previously described(More)
Skin is a major source of secretion of the neurotrophic factors nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial-derived neurotrophic factor (GDNF) controlling cutaneous sensory innervation. Beside their neuronal contribution, we hypothesized that neurotrophic factors also modulate the cutaneous(More)
Agents known to disrupt intraterminal Ca2+ buffering, N,N-dimethylamino-8-octyl-3,4,5-trimethoxybenzoate (TMB-8), 25 microM; caffeine, 7.5 mM; N,N-bis(3,4-dimethoxyphenethyl)-N-methylamine (YS035), 180 microM; ouabain, 200 microM; and dantrolene, 50 microM, were tested for the ability to alter effects of methyl mercury (MeHg) on spontaneous quantal release(More)
The interaction of methylmercury (MeHg) with various inhibitors of mitochondrial function (dinitrophenol, 50 microM; dicoumarol, 100 microM; valinomycin, 20 microM; and ruthenium red, 20 microM) on spontaneous quantal release of acetylcholine was tested at the neuromuscular junction of the rat. The objective was to determine whether these mitochondrial(More)
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