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• W1514264104 abstract "Embryonal period of ontogenesis plays an important role in the brain development which is defined, first of all, by genetical factors. Normal flow of the process can be disturbed also under the influence of many environmental factors which affect, both a differentiation of neurones, and on a neurotransmitter choice in them used for communications with the proximate cells (Le Douarin, 1981; Pendleton, 1998). The majority of the factors attacking developing brain during this period, break a normal ontogenesis of neurotransmitter systems: NA, 5-HT, DA and ACh that shows high sensitivity of a brain in critical periods of the development (Williams, 1992; Oliff, 1999; Qiao, 2004). A variety of neurochemical changes in the embryonic brain, induced by exposure to neurotropic compounds during the prenatal period, result in the development of functional impairments and behavioral disorders in the adult offspring. The mechanisms of action of many chemical factors on the developing fetal brain during early ontogenesis are in most cases mediated by alterations in the formation and functioning of brain neurotransmitter systems, including the cholinergic system, whose CNS function is associated with memory, learning, and behavioral processes (Yamada et al., 1986; Buzsaki, 1989; Everitt & Robbins, 1998; Levin & Slotkin, 1988; Zoli et al., 1999). During the period of neuron development, actions on cholinergic mechanisms lead to delays in cell differentiation which correlate with cognitive and behavioral deficits in fertile offspring (Yamada et al., 1986; Levin & Simon, 1998; Beer et al., 2005). Prenatal exposure to neurotoxins (nicotine, organochlorine compounds, barbiturates), which have cholinotropic properties, produces long-lasting changes in neurotransmitter functions in early ontogenesis with the subsequent development of neurobehavioral anomalies and affective disorders in pubescent individuals (Seidler et al., 1992; Barinaga, 1996; Slotkin, 2004). Thus, embryonic exposure to nicotine leads to alterations to cell proliferation and differentiation, resulting in long-term changes to synaptic function (Peters, 1986; Lichtensteiger, 1988). Binding to N-cholinergic receptors in catecholamine-containing neurons in the fetal brain, nicotine disrupts the expression of these transmitters" @default.
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• W1514264104 date "2011-12-22" @default.
• W1514264104 modified "2023-10-16" @default.
• W1514264104 title "Development of Male Sexual Function After Prenatal Modulation of Cholinergic System" @default.
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• W1514264104 doi "https://doi.org/10.5772/27552" @default.
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