Prenatal nicotine exposure affects the development of the central serotonergic system as well as the dopaminergic system in rat offspring: involvement of route of drug administrations

Muneoka, Katsumasa; Ogawa, Tetsuo; Kamei, Kaeko; Muraoka, Shin‐ichiro; Tomiyoshi, Rika; Mimura, Yuichi; Kato, Hitomi; Suzuki, Minoru; Takigawa, Morikuni

doi:10.1016/s0165-3806(97)00092-8

Cited by 124 publications

(81 citation statements)

References 33 publications

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“…It has been well documented that chronic prenatal nicotine exposure alters the development of DA neurons (Fung, 1988,Navarro et al, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Richardson and Tizabi, 1994,Muneoka et al, 1997. As suggested in the present study, one potential site of action for nicotine in producing these changes may be through direct action on nAChRs on immature DA neurons.…”

Section: Fetal Periodsupporting

confidence: 64%

“…As compared to P21, however, nicotine potency was an order of magnitude lower in fetal brain. This finding, combined with our observation of changing developmental patterns of subunit expression and radioligand binding, suggests that fetal DA terminals express a nAChR with different properties from that of older animals.It has been well documented that chronic prenatal nicotine exposure alters the development of DA neurons (Fung, 1988,Navarro et al, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Richardson and Tizabi, 1994,Muneoka et al, 1997. As suggested in the present study, one potential site of action for nicotine in producing these changes may be through direct action on nAChRs on immature DA neurons.…”

supporting

confidence: 64%

“…,Pliszka et al, 1996,Castellanos, 1997. In animal studies, maternal nicotine exposure produces sexdependent alterations in the development of DA neurochemical markers (Fung, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Muneoka et al, 1997, and induces hyperactivity in the offspring, which is believed to result from alterations in mesolimbic and nigrostriatal DA systems ,Fung and Lau, 1989,Richardson and Tizabi, 1994,Tizabi et al, 1997,Ajarem and Ahmad, 1998. However, one point of intense controversy is whether the actions of nicotine are mediated directly on DA neurons or are the result of indirect effects such as hypoxia (Slotkin, 1998).…”

mentioning

confidence: 99%

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Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

2007

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We have combined anatomical and functional methodologies to provide a comprehensive analysis of the properties of nicotinic acetylcholine receptors (nAChRs) on developing dopamine (DA) neurons. Double-labeling in situ hybridization was used to examine the expression of nAChR subunit mRNAs within developing midbrain DA neurons. As brain maturation progressed there was a change in the pattern of subunit mRNA expression within DA neurons, such that α3 and α4 subunits declined and α6 mRNA increased. Although there were strong similarities in subunit mRNA expression in substantia nigra (SNc) and ventral tegmental area (VTA), there was higher expression of α4 mRNA in SNc than VTA at gestational day (G)15, and of α5, α6 and β3 mRNAs during postnatal development. Using a superfusion neurotransmitter release paradigm to functionally characterize nicotine-stimulated release of [ 3 H]DA from striatal slices, the properties of the nAChRs on DA terminals were also found to change with age. Functional nAChRs were detected on striatal terminals at G18. There was a decrease in maximal release in the first postnatal week, followed by an increase in nicotine efficacy and potency during the second and third postnatal weeks. In the transition from adolescence (postnatal days (P) 30 and 40) to adulthood, there was a complex pattern of functional maturation of nAChRs in ventral, but not dorsal, striatum. In males, but not females, there were significant changes in both nicotine potency and efficacy during this developmental period. These findings suggest that nAChRs may play critical functional roles throughout DA neuronal maturation. Keywords adolescent; fetal; nicotine; sex; striatum; maternal smoking Maternal smoking during pregnancy has been correlated with a number of adverse outcomes in the offspring (Lichtensteiger et al., 1988,Lichtensteiger andSchlumpf, 1993), including cognitive deficits that are often manifested in early childhood as attention deficit hyperactivity disorder (ADHD) (Millberger et al., 1996). Though the underlying neurobiological mechanism * Correspondence to: Dr. Layla Azam Department of Biology, University of Utah 257 South 1400 East Salt Lake City, UT 84112 Tel.: (801) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ,Pliszka et al., 1996,Castellanos, 1997. In animal studies, maternal nicotine exposure produces sexdependent alterations in the development of DA neurochemical markers (Fung, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Muneoka et al., 1997, and induces hyperactivity in the offspring, which is believed...

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Section: Fetal Periodsupporting

confidence: 64%

supporting

confidence: 64%

mentioning

confidence: 99%

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Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

2007

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“…We know that dopaminergic and noradrenergic functions are affected by PNE (Navarro et al, 1990;Seidler et al, 1992;Slotkin, 1998), and that PNE alters morphology, volume, and dopamine turnover in medial prefrontal cortex (mPFC) (Muhammad et al, 2012;Muneoka et al, 1997;Mychasiuk et al, 2013;Schneider et al, 2011;Zhu et al, 2012), but we still do not understand how neural signals related to executive control mechanisms are affected. Although neighboring structures have been explored (Emeric et al, 2008;Hanes et al, 1998;Schall and Boucher, 2007), it is still unclear how firing in mPFC is normally modulated during tasks that probe response inhibition.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex

Bryden

Burton

Barnett

et al. 2015

Neuropsychopharmacol

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Prenatal nicotine exposure (PNE) is linked to numerous psychiatric disorders including attention deficit hyperactivity disorder (ADHD). Current literature suggests that core deficits observed in ADHD reflect abnormal inhibitory control governed by the prefrontal cortex. Yet, it is unclear how neural activity in the medial prefrontal cortex (mPFC) is modulated during tasks that assess response inhibition or if these neural correlates, along with behavior, are affected by PNE. To address this issue, we recorded from single mPFC neurons in control and PNE rats as they performed a stop-signal task. We found that PNE rats were faster for all trial-types, made more premature responses, and were less likely to inhibit behavior on 'STOP' trials during which rats had to inhibit an already initiated response. Activity in mPFC was modulated by response direction and was positively correlated with accuracy and movement time in control but not PNE rats. Although the number of single neurons correlated with response direction was significantly reduced by PNE, neural activity observed on general STOP trials was largely unaffected. However, dramatic behavioral deficits on STOP trials immediately following non-conflicting (GO) trials in the PNE group appear to be mediated by the loss of conflict monitoring signals in mPFC. We conclude that prenatal nicotine exposure makes rats impulsive and disrupts firing of mPFC neurons that carry signals related to response direction and conflict monitoring.

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“…Significant levels of acetylcholinesterase have been shown in the developing zebrafish nervous system (Hanneman and Westerfield, 1989). In the developing rat CNS, prenatal exposure to nicotine leads to impairments in the cholinergic, (Navarro et al, 1989), adrenergic (Navarro et al, 1990), dopaminergic, and serotonergic systems (Muneoka et al, 1997). Exposing hippocampal progenitor cells to low levels of nicotine causes rapid and selective apoptotic cell death of undifferentiated progenitor cells (Berger et al, 1998).…”

mentioning

confidence: 99%

Nicotinic Receptors Mediate Changes in Spinal Motoneuron Development and Axonal Pathfinding in Embryonic Zebrafish Exposed to Nicotine

Svoboda

Vijayaraghavan²,

Tanguay

2002

J. Neurosci.

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We show that transient exposure of embryonic zebrafish to nicotine delays the development of secondary spinal motoneurons. Furthermore, there is a long-lasting alteration in axonal pathfinding in secondary motoneurons that is not ameliorated by drug withdrawal. These effects of nicotine were reversed by mammalian nicotinic receptor antagonists. Coupled with these changes is a long-term alteration in swimming behavior. Our results show that transient embryonic exposure to nicotine leads to long-lasting effects on the vertebrate nervous system. These results also demonstrate that the zebrafish is a useful model to examine the effects of nicotine specifically, and drugs of abuse in general, on the development of the CNS in vertebrates.

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Prenatal nicotine exposure affects the development of the central serotonergic system as well as the dopaminergic system in rat offspring: involvement of route of drug administrations

Cited by 124 publications

References 33 publications

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex

Nicotinic Receptors Mediate Changes in Spinal Motoneuron Development and Axonal Pathfinding in Embryonic Zebrafish Exposed to Nicotine

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