Maternal exposure of rats to nicotine via infusion during gestation produces neurobehavioral deficits and elevated expression of glial fibrillary acidic protein in the cerebellum and CA1 subfield in the offspring at puberty

Chronic nicotine induces growth retardation in neonatal rat pups

“…Animal models have been used to study short-and long-term consequences of developmental nicotine exposure in an attempt to link nicotine to the observed adverse effects found in babies whose mothers smoked during pregnancy. The results confirmed several behavioral findings such as enhanced locomotor activity, neurobehavioral deficits and impaired cognition (Sobrian et al, 2003;Tizabi et al, 2000;Ajarem and Ahmad, 1998;Abdel-Rahman et al, 2005). However, although, nicotine's anorexic properties are well documented for adults Guan et al, 2004), a link between gestational nicotine and lower birth weight has not yet been established.…”

Effects of nicotine exposure during prenatal or perinatal period on cell numbers in adult rat hippocampus and cerebellum: A stereology study

“…Abdel- Rahman et al (2005) reported a decrease in surviving cerebellar Purkinje cell and hippocampal CA1 pyramidal cell densities (cell number/mm 2 ) following prenatal nicotine treatment. However, such findings were based on assessment using a cell counting method with certain sampling biases (e.g., counting cell or particle of interests only from a selected area within a histological section, and only from a few selected sections of a entire structure).…”

Prenatal Exposure to Nicotine Stimulates Neurogenesis of Orexigenic Peptide-Expressing Neurons in Hypothalamus and Amygdala

“…However, the mechanisms mediating this behavioral effect are unclear. Nicotine during gestation, generally tested at moderate to high doses, has suppressive effects on neurodevelopment in the forebrain, causing a decrease in cell number and survival, a decrease in neuronal area and number, and an increase in apoptotic cell death (Roy et al, 2002;Abdel-Rahman et al, 2005;Wei et al, 2011;Santiago and Huffman, 2012). With these effects accompanied by reduced functioning of two closely related dopaminergic and cholinergic neurochemical systems that mediate reward (Fung and Lau, 1989;Kane et al, 2004;Picciotto and Kenny, 2013), the resulting state of reward deficiency is suggested to increase the offspring's propensity to overconsume nicotine, raising dopamine to normal levels (Kane et al, 2004).…”