Alterations of brain tissue in fetal rats exposed to nicotine in utero: possible involvement of nitric oxide and catecholamines

Önal, Aytül; Uysal, Ayşegül; Ülker, Sibel; Delen, Yasemi̇n; Yurtseven, Mine; Evinç, Akgün

doi:10.1016/j.ntt.2003.08.005

Cited by 21 publications

(12 citation statements)

References 31 publications

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“…Gestational nicotine treatment has also been shown to decrease total numbers of cells in whole brain and in certain subregions, during the fetal and early neonatal period, consistent with a role of nAChRs in apotosis (Slotkin et al, 1987b; Onal et al, 2004). The activity of ornithine decarboxylase in neonatal rat brain is also increased by prenatal nicotine exposure, suggesting an abnormal switch from cellular proliferation to differentiation (Slotkin et al, 1987b; Navarro et al, 1989).…”

Section: Prenataldevelopmentmentioning

confidence: 77%

“…Chronic nicotine infusion also alters brain levels of dopamine, norepinephrine and their metabolites during the late prenatal period (Ribary and Lichtensteiger, 1989; Onal et al, 2004). In the early postnatal period, both dopamine and norepinephrine levels are elevated in the forebrain of rats treated with nicotine during gestation, although they return to control levels by adulthood (Ribary and Lichtensteiger, 1989).…”

Section: Prenataldevelopmentmentioning

confidence: 99%

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The dynamic effects of nicotine on the developing brain

Dwyer

McQuown

Leslie

2009

Pharmacology & Therapeutics

505

408

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Nicotinic acetylcholine receptors (nAChRs) regulate critical aspects of brain maturation during the prenatal, early postnatal, and adolescent periods. During these developmental windows, nAChRs are often transiently upregulated or change subunit composition in those neural structures that are undergoing major phases of differentiation and synaptogenesis, and are sensitive to environmental stimuli. Nicotine exposure, most often via tobacco smoke, but increasingly via nicotine replacement therapy, has been shown to have unique effects on the developing human brain. Consistent with a dynamic developmental role for acetylcholine, exogenous nicotine produces effects that are unique to the period of exposure and that impact the developing structures regulated by acetylcholine at that time. Here we present a review of the evidence, available from both the clinical literature and preclinical animal models, which suggests that the diverse effects of nicotine exposure are best evaluated in the context of regional and temporal expression patterns of nAChRs during sensitive maturational periods, and disruption of the normal developmental influences of acetylcholine. We present evidence that nicotine interferes with catecholamine and brainstem autonomic nuclei development during the prenatal period of the rodent (equivalent to first and second trimester of the human), alters the neocortex, hippocampus, and cerebellum during the early postnatal period (third trimester of the human), and influences limbic system and late monoamine maturation during adolescence.

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Section: Prenataldevelopmentmentioning

confidence: 77%

Section: Prenataldevelopmentmentioning

confidence: 99%

The dynamic effects of nicotine on the developing brain

Dwyer

McQuown

Leslie

2009

Pharmacology & Therapeutics

505

408

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“…Previous studies have shown that nicotine treatment not only causes swelling and structural remodeling of mitochondria in cells of various tissues, including the brain (Jin and Roomans 1997; Maritz and Thomas 1994; Onal et al 2004; Zimmerman and McGeachie 1987), but also regulates processes such as protein turnover (Katyare and Shallom 1988), enzyme activity (Barbieri et al 1989; Galvin et al 1988), and generation of ROS (Bhagwat et al 1998; Soto-Otero et al 2002). Here, we further demonstrate that the genes of each complex in the electron transfer system are modulated by chronic nicotine treatment.…”

Section: Discussionmentioning

confidence: 99%

Significant modulation of mitochondrial electron transport system by nicotine in various rat brain regions

et al. 2009

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The mitochondrion is the organelle responsible for generation of most usable energy in a cell. It also plays an important role in a series of physiological processes such as apoptosis and proliferation. Although previous studies have demonstrated that nicotine modulates the morphology and function of mitochondria, the mechanism(s) underlying these effects is largely unknown. In this study, using a microarray consisting of 4,793 clones derived from a mouse dopamine cDNA library, we profiled the gene expression patterns for six brain regions (amygdala, hippocampus, nucleus accumbens, prefrontal cortex, striatum, and ventral tegmental area) of female Sprague-Dawley rats subjected to nicotine treatment for 7 days through osmotic minipump infusion. We identified a number of genes and pathways, including components of the electron transport system of mitochondria, such as cytochrome c oxidase subunit I (Mt-co1), Mt-co2, Mt-co3, cytochrome b (Mt-cyb), mitochondrial NADH dehydrogenase 4 (Mt-nd4), and Mt-nd6, that were significantly modulated by nicotine in multiple brain regions. Bioinformatics analysis provided evidence that Gene Ontology categories related to the electron transport system were overrepresented in each brain region. Finally, the results from the microarray analysis were verified by quantitative RT-PCR for four representative genes. Together, our findings imply that mitochondria are involved in neuronal adaptation to chronic nicotine exposure.

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“…Progress has been made in demonstrating that programming during early development may impact on BP in later life (Vehaskari et al, 2001). In addition, it is known that nicotine, another cholinergic agent, can enter fetuses via mothers exposed to smoking (Onal et al, 2004;Oncken et al, 2003). Therefore, it is important to investigate the functional development of central cholinergic mechanisms controlling fetal cardiovascular homeostasis.…”

Section: Introductionmentioning

confidence: 99%

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

Shi

Morrissey

Yao

et al. 2005

Neuropsychopharmacol

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Central cholinergic mechanisms play important roles in the control of cardiovascular responses. However, in utero development of brain cholinergic mechanism in regulation of arterial pressure before birth is largely unknown. This study investigated cardiovascular responses to central application of carbachol in fetuses and determined functional development of the central cholinergic systems controlling fetal pressor responses in utero. Chronically prepared near-term ovine fetuses (90% gestation) received an injection of carbachol intracerebroventricularly (i.c.v.). Fetal cardiovascular responses were measured, and the brains were used for c-fos mapping studies. In response to carbachol injection i.c.v., fetal systolic, diastolic, and mean arterial pressure (MAP) immediately increased, accompanied by a bradycardia. The maximum increase of MAP was at 30 min after the i.c.v. injection of carbachol and lasted 90 min. Associated with the pressor response, the neuronal activity marked with c-fos was enhanced significantly in the fetal anterior third ventricle (AV3V) region (including the median preoptic nucleus and organum vasculosum of the lamina terminalis) in the forebrain, and in the area postrema, lateral parabrachial nucleus, nucleus tractus solitary, and rostral ventrolateral medulla in the hindbrain. These results indicate that the central cholinergic mechanism is functional in the control of fetal blood pressure at the last third of gestation, and the central AV3V region and hindbrain have been intact relatively during in utero development in sheep at 90% gestational stage.

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Alterations of brain tissue in fetal rats exposed to nicotine in utero: possible involvement of nitric oxide and catecholamines

Cited by 21 publications

References 31 publications

The dynamic effects of nicotine on the developing brain

The dynamic effects of nicotine on the developing brain

Significant modulation of mitochondrial electron transport system by nicotine in various rat brain regions

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

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