Cocaine‐induced neurodevelopmental deficits and underlying mechanisms

Martin, Melissa M.; Graham, Devon L.; McCarthy, Deirdre M.; Bhide, Pradeep G.; Stanwood, Gregg D.

doi:10.1002/bdrc.21132

Cited by 33 publications

(16 citation statements)

References 302 publications

(444 reference statements)

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“…However, we cannot rule out the potential contribution of isoflurane exposure to BDNF expression in the experimental and control groups in the present study. Prenatal cocaine exposure is reported to affect locomotor activity in rodent models [53]. However, we did not find significant changes in open field activity in our prenatal cocaine exposure mouse model (data not shown).…”

Section: Discussioncontrasting

confidence: 65%

Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model

McCarthy

Bell²,

Cannon

et al. 2016

Dev Neurosci

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Prenatal cocaine exposure remains a major public health concern because of its adverse impact on cognitive function in children and adults. We report that prenatal cocaine exposure produces significant deficits in reversal learning, a key component of cognitive flexibility, in a mouse model. We used an olfactory reversal learning paradigm and found that the prenatally cocaine-exposed mice showed a marked failure to learn the reversed paradigm. Because brain-derived neurotrophic factor (BDNF) is a key regulator of cognitive functions, and because prenatal cocaine exposure increases the expression of BDNF and the phosphorylated form of its receptor, tyrosine kinase B (TrkB), we examined whether BDNF-TrkB signaling is involved in mediating the reversal learning deficit in prenatally cocaine-exposed mice. Systemic administration of a selective TrkB receptor antagonist restored normal reversal learning in prenatally cocaine-exposed mice, suggesting that increased BDNF-TrkB signaling may be an underlying mechanism of reversal learning deficits. Our findings provide novel mechanistic insights into the reversal learning phenomenon and may have significant translational implications because impaired cognitive flexibility is a key symptom in psychiatric conditions of developmental onset.

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Section: Discussioncontrasting

confidence: 65%

Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model

McCarthy

Bell²,

Cannon

et al. 2016

Dev Neurosci

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“…Altered emotional reactivity, arousal and attention deficits later in life are the hallmarks of prenatal cocaine exposure (PCE), documented in multiple human studies These symptoms are also consistent with the acute effects of psychostimulant drugs, including cocaine . A meta‐analysis of 15 studies determined that, for cocaine users, impaired attention has the largest effect size of all cognitive effects of cocaine use .…”

Section: Introductionmentioning

confidence: 91%

Prenatal cocaine exposure disrupts the dopaminergic system and its postnatal responses to cocaine

Riley

Maymi

Pawlyszyn

et al. 2017

Genes Brain and Behavior

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Impaired attention is the hallmark consequence of prenatal cocaine exposure (PCE), affecting brain development, learning, memory and social adaptation starting at an early age. To date, little is known about the brain structures and neurochemical processes involved in this effect. Through focusing on the visual system and employing zebrafish as a model, we show that PCE reduces expression of dopamine receptor Drd1, with levels reduced in the optic tectum and other brain regions, but not the telencephalon. Organism-wide, PCE results in a 1.7-fold reduction in the expression of the dopamine transporter (dat), at baseline. Acute cocaine administration leads to a 2-fold reduction in dat in drug-naive larvae but not PCE fish. PCE sensitizes animals to an anxiogenic-like behavioral effect of acute cocaine, bottom-dwelling, while loss of DAT due to genetic knockout (DATKO) leads to bottom-dwelling behavior at baseline. Neuronal calcium responses to visual stimuli in both PCE and DATKO fish show tolerance to acute cocaine in the principal regions of visual attention, the telencephalon and optic tectum. The zebrafish model can provide a sensitive assay by which to elucidate the molecular mechanisms and brain region-specific consequences of PCE, and facilitate the search for effective therapeutic solutions.

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“…The association between cocaine exposure in second trimester and poor motor development in the infants based on psychomotor developmental index (PDI) was reported in a cohort study (Richardson et al, 2008). However, given that cocaine users frequently abuse other drugs and substances, the consequences of PCE at different stages of the trimester is not clearly defined (Martin et al, 2016).…”

Section: Cocainementioning

confidence: 99%

Prenatal Environment That Affects Neuronal Migration

Hwang

Hashimoto-Torii

2019

Front. Cell Dev. Biol.

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Migration of neurons starts in the prenatal period and continues into infancy. This developmental process is crucial for forming a proper neuronal network, and the disturbance of this process results in dysfunction of the brain such as epilepsy. Prenatal exposure to environmental stress, including alcohol, drugs, and inflammation, disrupts neuronal migration and causes neuronal migration disorders (NMDs). In this review, we summarize recent findings on this topic and specifically focusing on two different modes of migration, radial, and tangential migration during cortical development. The shared mechanisms underlying the NMDs are discussed by comparing the molecular changes in impaired neuronal migration under exposure to different types of prenatal environmental stress.

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Cocaine‐induced neurodevelopmental deficits and underlying mechanisms

Cited by 33 publications

References 302 publications

Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model

Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model

Prenatal cocaine exposure disrupts the dopaminergic system and its postnatal responses to cocaine

Prenatal Environment That Affects Neuronal Migration

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