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All experiments were carried out humanely and with regard for alleviation of suffering, with protocols approved by the Institutional Animal Care and Use Committee and in accordance with all federal and state guidelines.Timed-pregnant Sprague-Dawley rats were shipped on the second day of gestation by climate-controlled truck (total transit time Assays were conducted on each individual tissue, so that each determination represented a value from the corresponding brain region of one animal.

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In particular, we showed how drug therapies commonly used in preterm labor enhance the subsequent vulnerability of the developing brain to chlorpyrifos, a commonly-used organophosphate pesticide (Aldridge et al., 2005; Levin et al., 2014; Meyer et al., 2005; Rhodes et al., 2004; Slotkin et al., 2013, 2014a).

However, by far the most widely-encountered prenatal drug exposure is nicotine.

Given that human exposures to nicotine and chlorpyrifos are widespread, our results point to the creation of a subpopulation with heightened vulnerability.

We gave nicotine to pregnant rats throughout gestation at a dose (3 mg/kg/day) producing plasma levels typical of smokers; offspring were then given chlorpyrifos on postnatal days 1–4, at a dose (1 mg/kg) that produces minimally-detectable inhibition of brain cholinesterase activity.

The α4β2 n ACh R is the most abundant n ACh R subtype in the mammalian brain (Flores et al., 1992; Happe et al., 1994; Whiting and Lindstrom, 1987, 1988) and underlies the ability of ACh systems to release other neurotransmitters involved in reward, cognition and mood (Buisson and Bertrand, 2001, 2002; Dani and De Biasi, 2001; Fenster et al., 1999; Quick and Lester, 2002).

High-affinity choline transporters and Ch AT are both constitutive components of ACh nerve terminals but they differ in their regulatory mechanisms and hence in their functional significance.Maternal cigarette smoking during pregnancy is the single most identifiable and preventable cause of neonatal morbidity and mortality (Di Franza and Lew, 1995), and the nicotine contained in tobacco smoke produces abnormalities of brain development leading to neurobehavioral deficits such as attention deficit/hyperactivity disorder, conduct disorder and affective disorders (Ernst et al., 2001; Herrmann et al., 2008; Slotkin, 2008).Besides active maternal smoking, significant nicotine exposures occur through second-hand smoke or through the use of nicotine replacement products in smoking cessation, or more recently, through the use of “vaping” devices for inhaling nicotine.Nicotine’s direct actions on nicotinic acetylcholine receptors (n ACh Rs), preempt the timing and intensity of the natural trophic signals ordinarily controlled by acetylcholine (ACh), leading to abnormalities of neuronal cell replication, differentiation and synaptic connectivity (Dwyer et al., 2008; Hohmann and Berger-Sweeney, 1998; Lauder and Schambra, 1999; Slotkin, 2004, 2008).Likewise, chlorpyrifos and other organophosphates target ACh systems as one of their primary modes of action, involving not only inhibition of cholinesterase (the mechanism for systemic toxicity), but also mechanisms that compromise ACh receptors and cell signaling at exposures below the threshold for cholinesterase inhibition (Slotkin, 2004, 2005).Accordingly, in the present work, we examined the impact of fetal nicotine exposure on the subsequent effects of postnatal chlorpyrifos directed toward the development of ACh systems in the rat brain.

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