Developmental cannabinoid exposure: New perspectives on outcomes and mechanisms

Sobrian, Sonya K.

doi:10.1016/j.ntt.2016.10.010

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…Animal studies have confirmed that prenatal cannabinoid exposure results in learning and memory deficits that are consistent with the cognitive deficits observed in children who were prenatally exposed to cannabinoids (Campolongo et al, 2011). Impaired short-term memory, verbal reasoning, and attention and increased impulsivity and hyperactivity in early childhood as well as impairment in visual reasoning, problem-solving, sustained attention, and visual-motor coordination are reported (Sobrian, 2016). Studies on children of various ages suggest that prenatal exposure to high doses of marijuana can affect the learning of tasks as well as emotional outcomes (Day et al, 2006;Goldschmidt et al, 2000;Gray et al, 2005).…”

Section: Introductionsupporting

confidence: 59%

Effects of prenatal synthetic cannabinoid exposure on the cerebellum of adolescent rat offspring

Pinky

Majrashi

Fujihashi

et al. 2021

Heliyon

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Cannabis is the most commonly used illicit drug worldwide. Recently, cannabis use among young pregnant women has greatly increased. However, prenatal cannabinoid exposure leads to long-lasting cognitive, motor, and behavioral deficits in the offspring and alterations in neural circuitry through various mechanisms. Although these effects have been studied in the hippocampus, the effects of prenatal cannabinoid exposure on the cerebellum are not well elucidated. The cerebellum plays an important role in balance and motor control, as well as cognitive functions such as attention, language, and procedural memories. The aim of this study was to investigate the effects of prenatal cannabinoid exposure on the cerebellum of adolescent offspring. Pregnant rats were treated with synthetic cannabinoid agonist WIN55,212-2, and the offspring were evaluated for various cerebellar markers of oxidative stress, mitochondrial function, and apoptosis. Additionally, signaling proteins associated with glutamate dependent synaptic plasticity were examined. Administration of WIN55,212-2 during pregnancy altered markers of oxidative stress by significantly reducing oxidative stress and nitrite content. Mitochondrial Complex I and Complex IV activities were also enhanced following prenatal cannabinoid exposure. With regard to apoptosis, pP38 levels were significantly increased, and proapoptotic factor caspase-3 activity, pERK, and pJNK levels were significantly decreased. CB1R and GluA1 levels remained unchanged; however, GluN2A was significantly reduced. There was a significant decrease in MAO activity although tyrosine hydroxylase activity was unaltered. Our study indicates that the effects of prenatal cannabinoid exposure on the cerebellum are unique compared to other brain regions by enhancing mitochondrial function and promoting neuronal survival. Further studies are required to evaluate the mechanisms by which prenatal cannabinoid exposure alters cerebellar processes and the impact of these alterations on behavior.

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Section: Introductionsupporting

confidence: 59%

Effects of prenatal synthetic cannabinoid exposure on the cerebellum of adolescent rat offspring

Pinky

Majrashi

Fujihashi

et al. 2021

Heliyon

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“…Marijuana is the most extensively used illicit drug among pregnant women with recently reported national statistics indicating that approximately 5.2% of pregnant women use marijuana annually. In a recent national survey of the prevalence and patterns of substance use among pregnant women, 2.8% reported marijuana use during their first trimester of pregnancy (Sobrian, ). A recent study has reported that about 20% of pregnant women 24 years and younger tested positive for marijuana use (Young‐Wolff et al, ).…”

Section: Introductionmentioning

confidence: 99%

Ethanol and cannabinoids interact to alter behavior in a zebrafish fetal alcohol spectrum disorder model

Boa-Amponsem

Zhang

Mukhopadhyay

et al. 2019

Birth Defects Research

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Background: Recent work suggests that endocannabinoids (eCBs) may signal through the sonic hedgehog signaling pathway. We therefore hypothesized that combined ethanol and eCB exposure during defined stages of zebrafish embryogenesis will produce deficits comparable to human fetal alcohol spectrum disorder (FASD). Methods: Zebrafish embryos were exposed to ethanol or cannabinoid agonists alone or in combination at defined developmental stages and assessed for changes in brain morphology or expression of marker genes such as pax6a. Juvenile fish were then assessed for risk-taking/anxiety-like behavior using the novel tank dive test. Results: Either chronic or acute exposure to high doses of the CB1R agonist ACEA resulted in FASD phenotypes. However, acute subthreshold doses of CB1R agonist alone, or combined with 0.5% ethanol, did not induce morphological phenotypes, but did induce dysmorphogenesis when combined with acute 1% ethanol. Phenotypes were rescued using the CB1R antagonist SR141716A. In addition, JZL195, a dual inhibitor of FAAH and MAGL, two degradative enzymes for eCBs, induced FASD phenotypes in the presence of subthreshold ethanol, confirming the activation of common signaling pathways by ethanol and eCBs. We next analyzed the effects of ethanol and CB1R agonist on juvenile zebrafish behavior and show that ACEA or ethanol alone did not alter behavior, but combined ACEA and ethanol increased risk-taking behavior. Conclusions: These studies demonstrate that pathological and behavioral phenotypes associated with FASD are induced by exposure to CB1R agonists and suggest that combined exposure to lower levels of alcohol and marijuana may be capable of inducing FASD-like morphological and behavioral impairments.

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“…Marijuana is lipid soluble and able to cross the placenta and blood‐brain barrier to accumulate in foetal tissues including brain tissues . It is processed in the body through the endocannabinoid system, which may be involved in brain development through neurogenesis, differentiation, migration and neural circuit wiring . Data suggest that this system exists from the earliest stages of pregnancy, presenting multiple points of vulnerability to exposure of marijuana throughout gestation, although the exact processes of this system's development are still not completely understood in humans .…”

Section: Introductionmentioning

confidence: 99%

Effects of prenatal marijuana exposure on neuropsychological outcomes in children aged 1‐11 years: A systematic review

Sharapova

Phillips

Sirocco

et al. 2018

Paediatric Perinatal Epid

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Background. Normalization of medicinal and recreational marijuana use has increased the importance of fully understanding effects of marijuana use on individual- and population-level health, including prenatal exposure effects on child development. We undertook a systematic review of the literature to examine the long-term effects of prenatal marijuana exposure on neuropsychological function in children aged 1–11 years. Methods. Primary research publications were searched from Medline, Embase, PsychInfo, CINAHL EbscoHost, Cochrane Library, Global Health, and ERIC (1980–2018). Eligible articles documented neuropsychological outcomes in children 1–11 years who had been prenatally exposed to marijuana. Studies of exposure to multiple prenatal drugs were included if results for marijuana exposure were reported separately from other substances. Data abstraction was independently performed by two reviewers using a standardized protocol. Results. The eligible articles (n=21) on data from seven independent longitudinal studies, had high quality based on the Newcastle-Ottawa Scale. Some analyses found associations (p<0.05) between prenatal marijuana exposure and decreased performance on memory, impulse control, problem solving, quantitative reasoning, verbal development, and visual analysis tests; as well as increased performance on attention and global motion perception tests. Limitations included concurrent use of other substances among study participants, potential underreporting and publication biases, non-generalizable samples, and limited published results preventing direct comparison of analyses. Conclusions. The specific effects of prenatal marijuana exposure remain unclear and warrant further research. The larger number of neuropsychological domains that exhibit decreased versus increased psychological and behavioral functions suggest that exposure to marijuana may be harmful for brain development and function.

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Developmental cannabinoid exposure: New perspectives on outcomes and mechanisms

Cited by 5 publications

References 30 publications

Effects of prenatal synthetic cannabinoid exposure on the cerebellum of adolescent rat offspring

Effects of prenatal synthetic cannabinoid exposure on the cerebellum of adolescent rat offspring

Ethanol and cannabinoids interact to alter behavior in a zebrafish fetal alcohol spectrum disorder model

Effects of prenatal marijuana exposure on neuropsychological outcomes in children aged 1‐11 years: A systematic review

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