Prevalence and patterns of sensory processing behaviors in a large clinical sample of children with prenatal alcohol exposure

Jirikowic, Tracy; Thorne, John C.; McLaughlin, S.B.; Waddington, Tiffany; Lee, Adrian K. C.; Hemingway, Susan J Astley

doi:10.1016/j.ridd.2020.103617

Cited by 25 publications

(16 citation statements)

References 40 publications

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“…Evidence for transgenerationally passed behavioral deficits due to PrEE were also found in the Adhesive Removal task, where F1, F2 and F3 mice showed significant impairments in the time before adhesive removal across all three trials compared to controls. These data suggest a substantial impact of PrEE on sensorimotor integration and fine motor processing, mirroring that which is seen in the clinical FASD population ( Jirikowic et al, 2020 ). However, the extension of this clinically-relevant phenotype to the subsequent generations seen here suggests this novel phenomenon may also produce similar effects within the clinical population, which has yet to be fully examined for the potential, transgenerational effects of PrEE.…”

Section: Discussionsupporting

confidence: 57%

“…Humans with FASD display sensory processing deficits ( Jirikowic et al, 2020 ), increased risk-taking behavior and poor impulse control ( Furtado and Roriz ST de, 2016 ), as well as increased incidence of depression ( O’Connor et al, 2002 ). Here, we found rodent behavioral correlates that mirror these FASD phenotypes to be present within directly exposed offspring with extension to F2 and F3 generations.…”

Section: Discussionmentioning

confidence: 99%

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Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice

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Kozanian

Rohac

et al. 2022

Front. Cell Dev. Biol.

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Background: Fetal alcohol spectrum disorders (FASD) represent a leading cause of non-genetic neuropathologies. Recent preclinical evidence from suggests that prenatal ethanol exposure (PrEE), like other environmental exposures, may have a significant, transgenerational impact on the offspring of directly exposed animals, including altered neocortical development at birth and behavior in peri-pubescent mice. How these adverse behavioral outcomes are manifested within the brain at the time of behavioral disruption remains unknown.Methods: A transgenerational mouse model of FASD was used to generate up to a third filial generation of offspring to study. Using a multi-modal battery of behavioral assays, we assessed motor coordination/function, sensorimotor processing, risk-taking behavior, and depressive-like behavior in postnatal day (P) 20 pre-pubescent mice. Additionally, sensory neocortical area connectivity using dye tracing, neocortical gene expression using in situ RNA hybridization, and spine density of spiny stellate cells in the somatosensory cortex using Golgi-Cox staining were examined in mice at P20.Results: We found that PrEE induces behavioral abnormalities including abnormal sensorimotor processing, increased risk-taking behavior, and increased depressive-like behaviors that extend to the F3 generation in 20-day old mice. Assessment of both somatosensory and visual cortical connectivity, as well as cortical RZRβ expression in pre-pubescent mice yielded no significant differences among any experimental generations. In contrast, only directly-exposed F1 mice displayed altered cortical expression of Id2 and decreased spine density among layer IV spiny stellate cells in somatosensory cortex at this pre-pubescent, post weaning age.Conclusion: Our results suggest that robust, clinically-relevant behavioral abnormalities are passed transgenerationally to the offspring of mice directly exposed to prenatal ethanol. Additionally, in contrast to our previous findings in the newborn PrEE mouse, a lack of transgenerational findings within the brain at this later age illuminates the critical need for future studies to attempt to discover the link between neurological function and the described behavioral changes. Overall, our study suggests that multi-generational effects of PrEE may have a substantial impact on human behavior as well as health and well-being and that these effects likely extend beyond early childhood.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice

Bottom

Kozanian

Rohac

et al. 2022

Front. Cell Dev. Biol.

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“…There is a high prevalence of FASD; an estimated 2%-5% of school-aged children in the United States are affected by FASD (May et al, 2009(May et al, , 2014. A group of commonly observed deficits in FASD is impaired sensory processing (Jirikowic et al, 2020;Schneider et al, 2011). Sensory processing refers to the complex processes in the central nervous system linking sensory inputs and the corresponding behavioral output, the deficits of which in individuals with FASD are mainly characterized by over responsiveness to innocuous or irrelevant stimuli, impaired habituation, or difficulty in transitioning to a different/novel environment (Fjeldsted & Xue, 2019;Franklin et al, 2008;Jirikowic et al, 2008Jirikowic et al, , 2020Wengel et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Prenatal ethanol exposure impairs sensory processing and habituation of visual stimuli, effects normalized by postnatal environmental enrichment

Wang

Martin

Lei

et al. 2022

Alcoholism Clin & Exp Res

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Background Individuals with fetal alcohol spectrum disorders (FASD) often show processing deficits in all sensory modalities. Using an operant light reinforcement model, we tested whether prenatal ethanol exposure (PE) alters operant responding to elicit a contingent sensory stimulus—light onset (turning on the light) and habituation to this behavior in rats. We also explored whether postnatal environmental enrichment could ameliorate PE‐induced deficits. Methods Pregnant Sprague Dawley rats were gavaged twice/day with 0 or 3 g/kg/treatment ethanol (15% w/v) during gestational days 8–20, mimicking second‐trimester heavy PE in humans. The offspring were reared in a standard housing condition or an enriched condition. Adult male and female offspring underwent an operant light reinforcement experiment with either a short‐access or a long‐access procedure. A dishabituation test was also conducted to characterize the habituation process. Results In the short‐access procedure, PE led to increased operant responding to the contingent light onset in both sexes reared in the standard housing condition. Such an effect was not observed in rats reared in enriched conditions due to an overall decrease in responding. Moreover, rats reared in enriched conditions showed greater short‐term habituation. In the long access procedure, PE rats showed increased responding and impaired long‐term habituation. The long‐access procedure facilitated both short‐term and long‐term habituation in control and PE rats. Conclusion Prenatal ethanol exposure increases responding to contingent light onset and impairs the long‐term habituation process. The PE‐induced deficits were ameliorated by rearing in the enriched environment and increasing the duration and frequency of exposure to light onset. The PE‐induced effects are like increased sensation‐seeking, a subtype of sensory‐processing deficit that is often observed in individuals with FASD. Our findings could inform a suitable animal model for investigating the underlying mechanisms and possible intervention strategies for sensory deficits in FASD.

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“…Internal capsule axons are comprised of thalamocortical axons, corticothalamic axons, and corticospinal axons which are involved in proper sensory and motor processing. FASD commonly results in sensory processing difficulties, so we hypothesized these axon tracts would be influenced by prenatal alcohol exposure (PAE) 1 . As a metric of axon growth, we investigated how PAE affected axon crossing at a critical checkpoint along their trajectory, the corticostriatal boundary (CSB).…”

Section: Descriptionmentioning

confidence: 99%

Prenatal alcohol exposure alters axon formation and Robo/Slit guidance cue expression in the internal capsule at E15.5

Chi

Dewees

Scoville

et al. 2022

Preprint

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We previously showed the prenatal alcohol exposure (PAE) induced precocious growth of E15.5 internal capsule axons. We set out to further delineate which axon tracts were affected and a potential mechanism for this phenomenon. Pregnant Swiss Webster mice were exposed to saline or 20% ethanol via subcutaneous injection from embryonic days (E) 7.5 until E14.5. E15.5 embryos were captured via C-section and brains were either fixed for immunostaining or flash frozen for tissue punches. To identify internal capsule axons we performed immunohistochemistry using L1 antibody to visualize all internal capsule axons and NetrinG1 antibody to identify thalamocortical axons specifically. mRNA was extracted from tissue punches to visualize Slit1, Robo1, Slit2, and Robo2 gene expression levels via real time RT PCR. We found that L1-expressing axons exhibited increased axon crossing in females with the opposite effect in males and no difference in Netrin-G1-expressing axons. We also found PAE increased Robo1 mRNA. Taken together, our results indicate that PAE elicits specific effects on axon trajectories, potentially via the Slit/Robo guidance family of repellents and receptors. These findings add to the growing body of evidence demonstrating alcohol disruptions of axon growth and guidance during embryonic development that may contribute to connectivity errors that characterize Fetal Alcohol Spectrum Disorders.

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Prevalence and patterns of sensory processing behaviors in a large clinical sample of children with prenatal alcohol exposure

Cited by 25 publications

References 40 publications

Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice

Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice

Prenatal ethanol exposure impairs sensory processing and habituation of visual stimuli, effects normalized by postnatal environmental enrichment

Prenatal alcohol exposure alters axon formation and Robo/Slit guidance cue expression in the internal capsule at E15.5

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