Prenatal exposure to drugs: effects on brain development and implications for policy and education

Thompson, Barbara L.; Levitt, Pat; Stanwood, Gregg D.

doi:10.1038/nrn2598

Cited by 303 publications

(234 citation statements)

References 185 publications

(137 reference statements)

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“…Although some animal data suggest adverse neurodevelopment outcomes due to opiate exposure in early life, clinical data in humans remains insufficient and inconclusive [4,5]. Nevertheless, the few data available for morphine [6] and codeine [7] do not indicate teratogenic properties when used during the first trimester.…”

Section: Introductionmentioning

confidence: 99%

Use of tramadol in early pregnancy and congenital malformation risk

Källén

Reis

2015

Reproductive Toxicology

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Only few studies exist regarding the risk of a teratogenic effect of tramadol when used in early pregnancy. Using the Swedish Medical Birth Register, women (deliveries in 1997-2013) who had reported the use of tramadol in early pregnancy were identified. Maternal characteristics and concomitant drug use were analyzed. Among 1 682 846 women (1 797 678 infants), 1751 (1776 infants) had used tramadol, 96 of the infants had a congenital malformation and 70 of them were relatively severe. The adjusted odds ratio for a relatively severe malformation was 1.33 (95% CI 1.05-1.70). The odds ratios for cardiovascular defects (1.56, 95% CI 1.04-2.29) and for pes equinovarus (3.63, 95% CI 1.61-6.89) were significantly increased. The study suggests a teratogenic effect of tramadol but the risk increase is moderate.Word count: 128.

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Section: Introductionmentioning

confidence: 99%

Use of tramadol in early pregnancy and congenital malformation risk

Källén

Reis

2015

Reproductive Toxicology

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“…However, GAD1 suppression in limited periods of development or in restricted cell types has multiple consequences. Disrupting GABA signaling during early development alters cellular migration and cortical architecture in cell type-dependent ways (Aronne et al, 2011;Cuzon et al, 2008;Haas et al, 2013;Manent et al, 2007;Thompson et al, 2009;Wu et al, 2012). PV þ interneurons are selectively disrupted by exogenous GABA potentiation (Haas et al, 2013;Levav-Rabkin et al, 2010).…”

Section: Gene Effects Converge Onto Gaba System Developmentmentioning

confidence: 99%

Neurodevelopment, GABA System Dysfunction, and Schizophrenia

Schmidt

Mirnics

2014

Neuropsychopharmacol

196

130

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The origins of schizophrenia have eluded clinicians and researchers since Kraepelin and Bleuler began documenting their findings. However, large clinical research efforts in recent decades have identified numerous genetic and environmental risk factors for schizophrenia. The combined data strongly support the neurodevelopmental hypothesis of schizophrenia and underscore the importance of the common converging effects of diverse insults. In this review, we discuss the evidence that genetic and environmental risk factors that predispose to schizophrenia disrupt the development and normal functioning of the GABAergic system.

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“…These drugs are known to modify cell migration (2, 3) and synapse formation (4,5), resulting in improper wiring of neuronal circuits, ultimately leading to behavioral modifications in offspring later in life (6). There have been few studies about the effects on fetal neural development of other substances such as the naturally occurring adenosine receptor antagonist caffeine, which is ubiquitously consumed in coffee and tea.…”

Section: Introductionmentioning

confidence: 99%

Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice

et al. 2013

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pregnancy.longitudinal prospective human studies will be needed to evaluate the consequences of caffeine consumption during effects of adenosine receptor antagonists including caffeine on brain development in humans. Retrospective and neuronal types as well as impaired memory on certain types of memory tests. This study raises questions about the that adult offspring of pregnant mice treated with adenosine receptor antagonists had reduced numbers of certain antagonists were more susceptible to seizures when exposed to a seizure-inducing agent. They further demonstrated into target regions. They then showed that 1-week-old offspring of pregnant mice treated with adenosine receptor delayed the migration of specific populations of neurons during brain maturation, resulting in their delayed insertion They found that caffeine or an adenosine receptor antagonist that specifically blocks type 2A adenosine receptors added caffeine to the drinking water of female mice throughout pregnancy and lactation. Monique Esclapez, 1,2 † Christophe Bernard 1,2 * † Consumption of certain substances during pregnancy can interfere with brain development, leading to deleterious long-term neurological and cognitive impairments in offspring. To test whether modulators of adenosine receptors affect neural development, we exposed mouse dams to a subtype-selective adenosine type 2A receptor (A 2A R) antagonist or to caffeine, a naturally occurring adenosine receptor antagonist, during pregnancy and lactation. We observed delayed migration and insertion of g-aminobutyric acid (GABA) neurons into the hippocampal circuitry during the first postnatal week in offspring of dams treated with the A 2A R antagonist or caffeine. This was associated with increased neuronal network excitability and increased susceptibility to seizures in response to a seizure-inducing agent. Adult offspring of mouse dams exposed to A 2A R antagonists during pregnancy and lactation displayed loss of hippocampal GABA neurons and some cognitive deficits. These results demonstrate that exposure to A 2A R antagonists including caffeine during pregnancy and lactation in rodents may have adverse effects on the neural development of their offspring.

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Prenatal exposure to drugs: effects on brain development and implications for policy and education

Cited by 303 publications

References 185 publications

Use of tramadol in early pregnancy and congenital malformation risk

Use of tramadol in early pregnancy and congenital malformation risk

Neurodevelopment, GABA System Dysfunction, and Schizophrenia

Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice

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