Effects of prenatal marijuana exposure on child behavior problems at age 10

Goldschmidt, Lidush; Day, Nancy L.; Richardson, Gale A.

doi:10.1016/s0892-0362(00)00066-0

Cited by 314 publications

(197 citation statements)

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“…LTP was studied in hippocampal slices obtained from 40-day-old rats. Glutamate release was measured by microdialysis in 40-and 80-day-old rats as well as in hippocampal primary cell cultures obtained from pups born from dams exposed to WIN.Furthermore, because previous clinical findings have reported abnormal motor activity in children of mothers who used marijuana during pregnancy (3,19), the effect of prenatal WIN exposure on spontaneous motility was analyzed in infant (12-day-old), juvenile (40-day-old), and adult (80-day-old) offspring. …”

mentioning

confidence: 99%

Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

Mereu

Fà

Ferraro

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

185

153

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To investigate the possible long-term consequences of gestational exposure to cannabinoids on cognitive functions, pregnant rats were administered with the CB1 receptor agonist WIN 55,212-2 (WIN), at a dose (0.5 mg͞kg) that causes neither malformations nor overt signs of toxicity. Prenatal WIN exposure induced a disruption of memory retention in 40-and 80-day-old offspring subjected to a passive avoidance task. A hyperactive behavior at the ages of 12 and 40 days was also found. The memory impairment caused by the gestational exposure to WIN was correlated with alterations of hippocampal long-term potentiation (LTP) and glutamate release. LTP induced in CA3-CA1 synapses decayed faster in brain slices of rats born from WIN-treated dams, whereas posttetanic and shortterm potentiation were similar to the control group. In line with LTP shortening, in vivo microdialysis showed a significant decrease in basal and K ؉ -evoked extracellular glutamate levels in the hippocampus of juvenile and adult rats born from WIN-treated dams. A similar reduction in glutamate outflow was also observed in primary cell cultures of hippocampus obtained from pups born from mothers exposed to WIN. The decrease in hippocampal glutamate outflow appears to be the cause of LTP disruption, which in turn might underlie, at least in part, the long-lasting impairment of cognitive functions caused by the gestational exposure to this cannabinoid agonist. These findings could provide an explanation of cognitive alterations observed in children born from women who use marijuana during pregnancy. E ven though marijuana is the most widely used illegal drug among women at reproductive age, reports dealing with the effects of prenatal exposure to this substance of abuse on the length of gestation, fetal growth, and offspring behavior are still controversial (1-4). Confounding factors, such as possible impurities in the drug and concomitant tobacco smoking, may be responsible for inconsistencies in the results reported in studies to date (4, 5). It is likely that many of these conflicting results are due to methodological problems such as the measurement of neonatal outcomes and the context in which the research is conducted. More complex and less understood is the scenario concerning the possible long-term consequences of in utero exposure to cannabis derivatives on cognitive functions. In fact, data on this issue are sparse, and the identification of alterations in brain development and adult expression of cognitive and behavioral functions is far from definitive. These inconclusive results may depend on ethical, practical, and interpretative difficulties surrounding research with human subjects (4). In this regard, animal models provide a useful tool for examining the possible developmental and long-term effects of prenatal exposure to cannabinoids (CBs).Studies performed in adult rats have demonstrated the involvement of a specific CB receptor (CB1) highly expressed in many brain regions (6) in the reinforcing effects of CBs (7) and also in the disru...

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mentioning

confidence: 99%

Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

Mereu

Fà

Ferraro

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

185

153

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“…Longitudinal human studies have documented that prenatal marijuana-exposed children and young adults exhibit a variety of emotional, cognitive and behavioral deficits, such as deficit executive function, depression, anxiety, inattention and delinquency. 20,27,[48][49][50][51][52] Alterations of the PENK gene also suggest specific cannabis effects on discrete neural systems in the caudal striatum that could influence motor behavior. Preproenkephalin is primarily expressed in striatal medium spiny projection neurons which comprise the indirect pathway innervating the globus pallidus, whereas PDYN is primarily expressed in the direct pathway to the substantia nigra.…”

Section: Discussionmentioning

confidence: 99%

“…19 In humans, longitudinal studies have documented motor, social and cognitive disturbances in offspring who were exposed to cannabis prenatally. 20,21 Despite documented behavioral impairments, there is presently limited information about specific neurobiological consequences of prenatal cannabis exposure in humans. Recently, we observed altered amygdala dopamine D 2 receptor mRNA expression in human fetuses with prenatal cannabis exposure.…”

Section: Introductionmentioning

confidence: 99%

Discrete opioid gene expression impairment in the human fetal brain associated with maternal marijuana use

et al. 2006

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Fetal development is a period sensitive to environmental influences such as maternal drug use. The most commonly used illicit drug by pregnant women is marijuana. The present study investigated the effects of in utero marijuana exposure on expression levels of opioid-related genes in the human fetal forebrain in light of the strong interaction between the cannabinoid and opioid systems. The study group consisted of 42 midgestation fetuses from saline-induced voluntary abortions. The opioid peptide precursors (preprodynorphin and preproenkephalin (PENK)) and receptor (mu, kappa and delta) mRNA expression were assessed in distinct brain regions. The effect of prenatal cannabis exposure was analyzed by multiple regression controlling for confounding variables (maternal alcohol and cigarette use, fetal age, sex, growth measure and post-mortem interval). Prenatal cannabis exposure was significantly associated with increased mu receptor expression in the amygdala, reduced kappa receptor mRNA in mediodorsal thalamic nucleus and reduced preproenkephalin expression in the caudal putamen. Prenatal alcohol exposure primarily influenced the kappa receptor mRNA with reduced levels in the amygdala, claustrum, putamen and insula cortex. No significant effect of prenatal nicotine exposure could be discerned in the present study group. These results indicate that maternal cannabis and alcohol exposure during pregnancy differentially impair opioid-related genes in distinct brain circuits that may have long-term effects on cognitive and emotional behaviors.

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“…Some evidence has shown that prenatal exposure leads to decreased IQ scores, cognitive function, and attention [11][12][13][14]. Day and colleagues found negative effects on prenatal marijuana exposure (mostly in first and second trimesters) with negative performance demonstrated in 3-year-old children on the Stanford-Binet Intelligence Scores [11].…”

Section: Pregnancy and Breastfeedingmentioning

confidence: 99%

“…Day and colleagues found negative effects on prenatal marijuana exposure (mostly in first and second trimesters) with negative performance demonstrated in 3-year-old children on the Stanford-Binet Intelligence Scores [11]. Goldschmidt and colleagues found increased hyperactivity, impulsivity, and inattention symptoms as measured by the Swanson, Noland, and Pelham (SNAP) checklist at age 10 in children with prenatal marijuana exposures [12]. Two cohort studies (Wilford, Fried) found deficits in visual-motor coordination, processing speed, visual memory, and interhemispheric transfer of information as late as adolescence after prenatal exposure [13,14].…”

Section: Pregnancy and Breastfeedingmentioning

confidence: 99%

Pediatric Concerns Due to Expanded Cannabis Use: Unintended Consequences of Legalization

Wang

2016

J. Med. Toxicol.

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An "unintended consequence" of marijuana legalization is the impact on the pediatric population. From prenatal exposure to unintentional childhood exposures, through concerns of adolescence abuse and marijuana use for medicinal indications in children, marijuana exposure can affect pediatric patients at every stage in childhood. Regardless of the stage or reason of exposure, concerns exist about short-term and long-term consequences in a child's physical and mental health. The use of cannabidiol (CBD) may have some benefit for the treatment of epilepsy, but emphasis needs to be on rigorous clinical trials to evaluate efficacy and safety. As more states allow both medical and recreational marijuana, availability and prevalence of use will likely increase and more surveillance and research is needed to evaluate the consequences on the pediatric population.

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Effects of prenatal marijuana exposure on child behavior problems at age 10

Cited by 314 publications

References 31 publications

Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

Discrete opioid gene expression impairment in the human fetal brain associated with maternal marijuana use

Pediatric Concerns Due to Expanded Cannabis Use: Unintended Consequences of Legalization

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