Effects of Gestational Nicotine Exposure on Hippocampal Morphology

Roy, Tara Sankar; Sabherwal, U.

doi:10.1016/s0892-0362(97)00137-2

Cited by 83 publications

(52 citation statements)

References 42 publications

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“…Only neurons with distinct nuclei were used for measurements. Correction for the split cell thickness was not applied as none of the neurons under the study was more than 25 μm in diameter (Roy and Sabherwal, 1998). Three random counting frames (1/100 mm 2 ) per section were selected for measuring the neuronal packing density.…”

Section: Morphological Analysismentioning

confidence: 99%

“…Three random counting frames (1/100 mm 2 ) per section were selected for measuring the neuronal packing density. The packing density was calculated as neurons per cubic millimeter in DG, CA1 and CA3 of hippocampus and the IGL, EGL and PC of cerebellum (Roy and Sabherwal, 1998). The calculation is: the number of cell / mm 3 = the number of cell in the counting frame / [5*10 -3 mm (section thickness) * 1/100 mm 2 (area of counting frame)].…”

Section: Morphological Analysismentioning

confidence: 99%

“…However, studies did reveal that prenatal nicotine exposure can result in altered morphological features in hippocampus and cortex (Roy et al, 2002,Roy andSabherwal 1998), and can interfere with long-term neuronal survival (Abdel-Rahman et al, 2005). Other studies focusing on receptor expression also showed upregulation of nAChR binding sites, mostly α4β2* nAChRs (Sugiyama et al, 1985;Cairns and Wonnacott, 1988;van de Kamp and Collins, 1994;Miao et al, 1998;Eriksson et al, 2000;Mugnaini et al, 2002a).…”

Section: Introductionmentioning

confidence: 99%

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Effects of chronic neonatal nicotine exposure on nicotinic acetylcholine receptor binding, cell death and morphology in hippocampus and cerebellum

2007

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Nicotine, the major psychoactive ingredient in tobacco interacting with nicotinic acetylcholine receptors (nAChR), is believed to have neuroprotective and neurotoxic effects on the developing brain. Neurotoxicity has been attributed to activation of homomeric α7 nAChRs, neuroprotection to heteromeric α4β2 nAChRs. Thus, developmental nicotine could have opposite effects in different brain regions, depending on nAChR subtype expression. Here, we determined if chronic neonatal nicotine exposure (CNN), during a period of brain growth corresponding to the third human trimester, differentially regulates nAChR expression, cell death, and morphological properties in hippocampus and cerebellum, two structures maturing postnatally. Rat pups were orally treated with 6 mg/kg/day nicotine from postnatal day (P)1 to P7. On P8, expression for α4, α7 and β2 mRNA was determined by in situ hybridization; nAChR binding sites in by receptor autoradiography, dying neurons by TUNEL and Fluoro-Jade staining and morphological properties by analysis of Cresyl-Violet stained sections. In control cerebellum, strong expression of α4, β2 mRNA and heteromeric nAChRs labeled with [ 125 I]-Epibatidine were found in granule cells, and α7 mRNA and homomeric nAChRs labeled with [ 125 I]-αBungarotoxin in the external germinal layer. In control hippocampus, low expression of α4 mRNA and heteromeric nAChRs and high expression of α7 mRNA and homomeric nAChRs were detected. CNN increased heteromeric nAChR binding in hippocampus but not cerebellum and significantly decreased neuronal soma size and increased packing density in hippocampal principal cells but not in cerebellum. CNN did not increase the number of dying cells in any area, but significantly fewer TUNEL-labeled cells were found in CA3 strata oriens and radiatum and cerebellar granule layer. Thus, the hippocampus seems to be more sensitive than the cerebellum to CNN which could result from different nAChR subtype expression and might explain long-lasting altered cognitive functions correlated with gestational nicotine exposure due to changes in hippocampal cell morphology.

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Section: Morphological Analysismentioning

confidence: 99%

Section: Morphological Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of chronic neonatal nicotine exposure on nicotinic acetylcholine receptor binding, cell death and morphology in hippocampus and cerebellum

2007

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“…Additionally, dendrite formation is known to be a highly dynamic process required for synaptogenesis and neuronal communication [for a review, see Whitford et al, 2002]. Numerous perinatal insults have been shown to affect dendrite outgrowth in the rat brain including perinatal exposure to nicotine [Roy and Sabherwal, 1998], monosodium glutamate [Gonzá lez-Burgos et al, 2001] and ethanol [Yanni and Lindsley, 2000], in addition to chronic placental insufficiency [Dieni and Rees, 2003] and early postnatal malnutrition [Cordero et al, 2003]. Given the susceptibility of dendritic growth to numerous perinatal insults in conjunction with decreased metabolism occurring during the hippocampal growth spurt, we hypothesized that perinatal iron deficiency negatively affects dendritic growth in the hippocampus, as evidenced by the cytoskeletal protein microtubule-associated protein-2 (MAP-2).…”

Section: Introductionmentioning

confidence: 99%

Perinatal Iron Deficiency Alters Apical Dendritic Growth in Hippocampal CA1 Pyramidal Neurons

Jorgenson

Wobken

Georgieff³

2003

Dev Neurosci

180

179

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Iron deficiency early in life is associated with cognitive disturbances that persist beyond the period of iron deficiency. Within cognitive processing circuitry, the hippocampus is particularly susceptible to insults during the perinatal period. During the hippocampal growth spurt, which is predominantly postnatal in rodents, iron transport proteins and their messenger RNA stabilizing proteins are upregulated, suggesting an increased demand for iron import during this developmental period. Rat pups deprived of iron during the perinatal period show a 30–40% decrease in hippocampal metabolic activity during postnatal hippocampal development. We hypothesized that this reduced hippocampal neuronal metabolism impedes developmental processes such as neurite outgrowth. The goals of the current study were to investigate the effects of perinatal iron deficiency on apical dendritic segment growth in the postnatal day (P) 15 hippocampus and to determine if structural abnormalities persist into adulthood (P65) following iron treatment. Qualitative and quantitative immunohistochemical analyses of dendritic structure and growth using microtubule-associated protein-2 as an index showed that iron-deficient P15 pups have truncated apical dendritic morphology in CA1 and a persistence of an immature apical dendritic pattern at P65. These results demonstrate that perinatal iron deficiency disrupts developmental processes in the hippocampal subarea CA1 and that these changes persist despite iron repletion. These structural abnormalities may contribute to the learning and memory deficits that occur during and following early iron deficiency.

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“…Los estudios en animales de laboratorio señalan la presencia de alteraciones funcionales y estructurales en diversas zonas cerebrales 61 tales como déficits en la función dopaminérgica del córtex frontal y alteraciones estructurales del hipocampo (áreas CA3 y CA1) 70,71 . La relación entre exposición prenatal al tabaco, el desarrollo de anomalías estructurales o funcionales del SNC y la existencia de disfunciones cognitivas y conductuales de diverso tipo es biológicamente plausible 66 , en la misma medida en que lo es para otras sustancias de abuso y en especial dadas las extensas interacciones funcionales entre los sistemas adrenérgicos y catecolaminérgicos 2 .…”

Section: Tabacounclassified

Maternidad, infancia y drogas: implicaciones clínicas

Botella¹

2004

Adicciones

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RESUMENObjetivos: Revisar la relación entre la exposición prenatal a drogas y el pronóstico fetal, neonatal e infantil. Material y méto-dos: se estudia el estado actual de la investigación relativa a la exposición prenatal a sustancias psicoactivas, mediante una extensa revisión de Medline y de las investigaciones de organismos norteamericanas y europeos durante los últimos años. Se presta especial atención a las dificultades metodológicas derivadas del objeto de estudio y a otros factores tales como la relación materno-infantil y las características de la mujer adicta. Resultados: la exposición prenatal a drogas se asocial a un amplio rango de complicaciones obstétricas y alteraciones neuroconductuales infantiles. Con la excepción del síndrome alcohólico fetal y otros efectos fetales ligados al alcohol, estas alteraciones suelen encontrarse en dominios cognitivos específicos y pueden estar moduladas por factores psicosociales y ambientales. Conclusiones: los niños expuestos prenatalmente a drogas pueden ser considerados un caso especial de infancia en riesgo. Es necesario investigar el impacto real de la exposición prenatal a sustancias psicoactivas y la relevancia de otros factores en su pronóstico a medio y largo plazo. Asimismo, es necesario implicar y formar a diferentes profesionales, tales como obstetras, ginecólogos y pediatras, y coordinar la intervención de las diferentes instituciones, para mejorar la atención prestada a la mujer drogodependiente y a sus hijos.Palabras clave: mujer, droga, teratógeno, embarazo de alto riesgo, manifestaciones neuroconductuales.

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Effects of Gestational Nicotine Exposure on Hippocampal Morphology

Cited by 83 publications

References 42 publications

Effects of chronic neonatal nicotine exposure on nicotinic acetylcholine receptor binding, cell death and morphology in hippocampus and cerebellum

Effects of chronic neonatal nicotine exposure on nicotinic acetylcholine receptor binding, cell death and morphology in hippocampus and cerebellum

Perinatal Iron Deficiency Alters Apical Dendritic Growth in Hippocampal CA1 Pyramidal Neurons

Maternidad, infancia y drogas: implicaciones clínicas

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