Cocaine causes deficits in radial migration and alters the distribution of glutamate and GABA neurons in the developing rat cerebral cortex

Lee, Chun-Ting; Chen, Jia; Worden, Lila; Freed, William J.

doi:10.1002/syn.20814

Cited by 34 publications

(37 citation statements)

References 76 publications

(102 reference statements)

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“…Kosofsky, on the other hand, has studied prenatal cocaine in a dose-response fashion in the mouse and found long term effects on cocaine reward that can be summarized as increasing the sensitivity to cocaine assessed by operant behavior and reducing the sensitivity to cocaine measured with classical conditioning such as CPP (Rocha et al 2002; Malanga et al 2007). These findings can be interpreted as selective effects of prenatal cocaine on descending cortical projections perhaps mediated by altered neural development in cerebral cortex (Lee et al 2011). …”

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confidence: 99%

The effects of prenatal cocaine, post-weaning housing and sex on conditioned place preference in adolescent rats

et al. 2014

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Rationale Gestational exposure to cocaine now affects several million people including adolescents and young adults. Whether prenatal drug exposures alter an individual's tendency to take and/or abuse drugs is still a matter of debate. Objectives This study sought to answer the question does prenatal exposure to cocaine, in a dose-response fashion, alter the rewarding effects of cocaine using a conditioned place preference (CPP) procedure during adolescence in the rat. Further, we wanted to assess possible sex differences and the role of being raised in an enriched vs impoverished environment. Methods Virgin female Sprague-Dawley rats were dosed daily with cocaine at 30mg/kg (C30), 60mg/kg (C60) or vehicle intragastrically prior to mating and throughout gestation. Pups were culled, fostered and on postnatal day (PND) 23 placed into isolation cages or enriched cages with 3 same-sex littermates and stimulus objects. On PND43-47, CPP was determined across a range of cocaine doses. Results C30 exposure increased sensitivity to the rewarding effects of cocaine in adolescent males and being raised in an enriched environment further enhanced this effect. Rats exposed to C60 resembled the controls in cocaine CPP. Overall, females were modestly affected by prenatal cocaine and enrichment. Conclusions These data support the unique sensitivity of males to the effects of gestational cocaine, that moderate prenatal cocaine doses produce greater effects on developing reward circuits than high doses, and that housing condition interacts with prenatal treatment and sex such that enrichment increases cocaine CPP most in adolescent males prenatally exposed to moderate cocaine doses.

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confidence: 99%

The effects of prenatal cocaine, post-weaning housing and sex on conditioned place preference in adolescent rats

et al. 2014

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“…Consistent with these primate studies, during periods of early neocorticogenesis in rodents, defined by mitotically active neural progenitor cells in the ventricular zone (VZ), cocaine inhibits growth of the neocortex and disrupts the distribution of glutamate and GABAergic neurons [18] .…”

Section: Research Highlightmentioning

confidence: 68%

Modeling cocaine-induced alterations in organization and patterning of neocortical development using human pluripotent stem cells

Lee¹,

Kindberg²,

Freed³

et al. 2015

Stem Cell Transl Invest

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Disorders of human neocortical development are particularly difficult to study by using animal models because of the marked complexity and unique features of the human cerebral cortex. Developmental effects of cocaine, as well as other drugs and toxins, are particularly challenging to study due to complicating factors such as variations in genetic background, time of exposure, and exposure to multiple substances. Studies aimed at elucidating the effects of cocaine on fetal brain development have used rodent cell lines, primary human cells, and rat models to show that cocaine metabolism by cytochrome P450 results in oxidative ER stress and subsequent impairment of neural progenitor cell proliferation. Recently, in vitro models of neocortical development have been generated by using pluripotent stem cells. One such model, utilizing human pluripotent stem cells, reproduced the formation of neocortical glutamatergic and GABAergic neurons on radial glial scaffolding structure in a temporally sensitive manner mimicking human in vivo neocortical development. Cocaine exposure resulted in the accumulation of reactive oxygen species (ROS), premature neuronal differentiation, accelerated development of deep-and upper-layer glutamatergic neurons, and increased formation of GABAergic interneurons. Each of these changes was inhibited by the cytochrome P450 inhibitor cimetidine. These studies suggest that, in the developing human cerebral cortex, cocaine metabolism through cytochrome P450-dependent ROS generation leads to premature neuronal differentiation of neocortical progenitors and impaired neocortical patterning. Although the overall organization of the neocortex is similar in all mammals, the complexity of the human cortex is unique, and is arguably the anatomical feature that most clearly distinguishes humans from other animals [1,2] . During neocortical development, forebrain cortical progenitors are sequentially specified to form various neuronal subtypes, and subsequently form the stereotypic layered cortical structure [3] . Due to vast differences between the human neocortex and that of frequently used model systems, rodents in particular, a human cell-based in vitro model, that preserves the essential spatial and temporal processes involved in neocortical development has recently been developed by Kindberg and coworkers [4] . This model has the potential to enable mechanistic studies of human neocorticogenesis, and thereby to provide new avenues for drug discovery and treatment of certain neurological disorders. RESEARCH HIGHLIGHT

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“…In nonhuman primates, it has been shown that prenatal COC administration resulted initially in a decrease in cell production within the fetal pseudostratified ventricular epithelium, which was then followed by an increase in neurogenesis (Lidow and Song, 2001). Lee et al (2011) suggested that COC may inhibit neuronal differentiation during cortical neurogenesis and the migration of glutamate and γ-aminobutyric acid (GABA) neurons, alterations that could potentially explain language delays and motor-development impairments.…”

Section: Dendritic Cell Architecturementioning

confidence: 99%

“…Prenatal COC exposure affects various neurotransmitters, including 5-HT, DA, NE, and glutamate (Henderson et al, 1991;Keller and SnyderKeller, 2000;Lee et al, 2011).…”

Section: Neurotransmitter Alterationsmentioning

confidence: 99%

Prenatal cocaine exposure and its impact on cognitive functions of offspring: a pathophysiological insight

Gkioka

Korou

Daskalopoulou

et al. 2016

Reviews in the Neurosciences

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It is estimated that approximately 0.5%-3% of fetuses are prenatally exposed to cocaine (COC). The neurodevelopmental implications of this exposure are numerous and include motor skill impairments, alterations of social function, predisposition to anxiety, and memory function and attention deficits; these implications are commonly observed in experimental studies and ultimately affect both learning and IQ. According to previous studies, the clinical manifestations of prenatal COC exposure seem to persist at least until adolescence. The pathophysiological cellular processes that underlie these impairments include dysfunctional myelination, disrupted dendritic architecture, and synaptic alterations. On a molecular level, various neurotransmitters such as serotonin, dopamine, catecholamines, and γ-aminobutyric acid seem to participate in this process. Finally, prenatal COC abuse has been also associated with functional changes in the hormones of the hypothalamic-pituitary-adrenal axis that mediate neuroendocrine responses. The purpose of this review is to summarize the neurodevelopmental consequences of prenatal COC abuse, to describe the pathophysiological pathways that underlie these consequences, and to provide implications for future research in the field.

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Cocaine causes deficits in radial migration and alters the distribution of glutamate and GABA neurons in the developing rat cerebral cortex

Cited by 34 publications

References 76 publications

The effects of prenatal cocaine, post-weaning housing and sex on conditioned place preference in adolescent rats

The effects of prenatal cocaine, post-weaning housing and sex on conditioned place preference in adolescent rats

Modeling cocaine-induced alterations in organization and patterning of neocortical development using human pluripotent stem cells

Prenatal cocaine exposure and its impact on cognitive functions of offspring: a pathophysiological insight

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