Smoking During Pregnancy and Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type: A Case-Control Study

Schmitz, Marcelo; Denardin, Daniel; Silva, Tatiana Laufer; Pianca, Thiago Gatti; Hutz, Mara Helena; Faraone, Stephen V.; Rohde, Luis Augusto

doi:10.1097/s0890-8567(09)61916-x

Cited by 103 publications

(77 citation statements)

References 45 publications

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“…Maternal smoking is a risk factor for many psychiatric disorders (Blood-Siegfried and Rende, 2010;Button et al, 2007;Ernst et al, 2001;Fried and Watkinson, 2001;Jacobsen et al, 2007;Milberger et al, 1996Milberger et al, , 1998Pauly and Slotkin, 2008;Schmitz et al, 2006;Thapar et al, 2003;Tong and McMichael, 1992) and is still a common practice according to Substance Abuse & Mental Health Services which reported in 2012 that one in five women smoke during pregnancy. In addition to being an important issue in its own right, prenatal nicotine exposure has gained considerable traction as a suitable model for impulsive behavior as seen in ADHD.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex

Bryden

Burton

Barnett

et al. 2015

Neuropsychopharmacol

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“…Nicotine from maternal cigarette smoking tends to accumulate in the fetal brain because of its higher lipid content and the lower clearance of nicotine from the fetal compartment (Lambers and Clark, 1996). Prenatal exposure to nicotine is strongly associated with an increased incidence of attention deficit disorder (Langley et al, 2005;Schmitz et al, 2006). It has been suggested that there are many similarities between brain development in young postnatal rats and in the third-trimester human fetus.…”

Section: Prenatal Nicotine Exposure and Attention Deficitsmentioning

confidence: 99%

“…Cortical nicotinic acetylcholine receptors are important for attention and effortful concentration (Rezvani and Levin, 2001;Granon et al, 2003;Lambe et al, 2005), and have been suggested to have long-lasting effects on the development of attention circuitry (Langley et al, 2005;Rodriguez and Bohlin, 2005;Schmitz et al, 2006). Abnormalities in cortical nicotinic binding have been demonstrated in several neurodevelopmental conditions, including autism (Perry et al, 2001;Martin-Ruiz et al, 2004), epilepsy (Picard et al, 2006), and schizophrenia (Breese et al, 2000;Marutle et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Developmental Excitation of Corticothalamic Neurons by Nicotinic Acetylcholine Receptors

Kassam¹,

Herman²,

Goodfellow³

et al. 2008

J. Neurosci.

129

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In this study, we show robust nicotinic excitation of pyramidal neurons in layer VI of prefrontal cortex. This layer contains the corticothalamic neurons, which gate thalamic activity and play a critical role in attention. Our experiments tested nicotinic excitation across postnatal development, using whole-cell recordings in prefrontal brain slices from rats. These experiments showed that layer VI neurons have peak nicotinic currents during the first postnatal month, a time period of intensive cortical development in rodents. We demonstrate that these currents are mediated directly by postsynaptic nicotinic receptors and can be suppressed by a competitive antagonist of ␣ 4 ␤ 2 * nicotinic receptors. To record from identified corticothalamic neurons, we performed stereotaxic surgery to label the neurons projecting to medial dorsal thalamus. As hypothesized, recordings from these retrogradely labeled neurons in layer VI showed prominent nicotinic currents. Finally, we examined the effects of the drug nicotine on layer VI neurons and probed for the potential involvement of the accessory subunit, ␣ 5 , in their receptors. A level of nicotine similar to that found in the blood of smokers elicits a stable inward current in layer VI neurons, yet this exposure desensitizes ϳ50% of the subsequent current elicited by acetylcholine. An allosteric modulator of ␣ 4 ␤ 2 ␣ 5 receptors resulted in a 2.5-fold potentiation of submaximal nicotinic currents. This result is consistent with the expression of the relatively rare ␣ 5 nicotinic subunit in layer VI. In summary, we show that layer VI corticothalamic neurons can be strongly excited during development by an unusual subtype of nicotinic receptor.

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“…Exposure to alcohol and nicotine during pregnancy has been related to an increased ADHD risk (29,30).…”

Section: How Does the Correlation Between Attention Deficit-hyperactimentioning

confidence: 99%

Comorbidity of attention deficit-hyperactivity disorder and substance use disorder

Evren¹

2018

Dusunen Adam

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Smoking During Pregnancy and Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type: A Case-Control Study

Cited by 103 publications

References 45 publications

Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex

Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex

Developmental Excitation of Corticothalamic Neurons by Nicotinic Acetylcholine Receptors

Comorbidity of attention deficit-hyperactivity disorder and substance use disorder

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