Evidence map›Paper›PMID 40128475›Full record

ReviewAdvances in experimental medicine and biology2025

Impact of Developmental Alcohol Exposure on the Thalamus.

C Fernando Valenzuela, Natalie M Reid, Benjamin B Blanco, Victoria L Carlson, Alynna B Do

Abstract readReview
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In one paragraph

Review in Advances in experimental medicine and biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

C Fernando ValenzuelaDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA. fvalenzuela@salud.unm.edu.
Natalie M ReidDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Benjamin B BlancoDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Victoria L CarlsonDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Alynna B DoDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.

Funding

Understanding neurophysiological deficits in response inhibition in children with FASDP50AA022534 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2014 to 2026
$21.5M
Alcohol and Developing Neuronal CircuitsR01AA015614 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2005 to 2026
$3.9M
NIAAA NIH HHS P50 AA022534NIAAA NIH HHS R01 AA015614
6 · The paper itself

Abstract

This chapter comprehensively explores the impact of prenatal alcohol (ethanol) exposure (PAE) on the thalamus, integrating findings from animal models and human studies spanning various developmental stages. Animal model investigations, encompassing first and second trimester-equivalent exposures and the critical third trimester, where the brain growth spurt starts, reveal specific alterations in thalamic structures and circuits, emphasizing the specificity of damage to corticothalamic loops. The ventrobasal thalamic nucleus exhibits a unique response to PAE, involving intricate interactions with postnatal neurogenesis and neurotrophin responsiveness. Third trimester-equivalent exposure consistently induces apoptotic neurodegeneration in various thalamic nuclei, highlighting the heightened susceptibility of the visual thalamus, particularly the lateral geniculate nucleus, during critical developmental periods. The nucleus reuniens, vital for cognitive processes, was shown to be significantly affected by alcohol exposure during this period. Investigations into the trigeminal/somatosensory system activity revealed disruptions in glucose utilization and increased neuronal activity in the thalamus. Research on binge-like alcohol exposure during the brain growth spurt demonstrates lasting modifications in action-potential properties and synaptic currents in thalamic neurons projecting to the retrosplenial cortex. Human studies, employing advanced techniques like super-resolution fetal MRI and functional MRI, underscore the PAE-induced structural and functional consequences in the thalamus and its connections, spanning from fetal development to adulthood. The complex effects of PAE on thalamic structure and function vary across developmental stages, emphasizing the importance of considering factors such as age and concurrent exposures. The development of higher-resolution imaging tools is essential for assessing the impact of PAE on the structure and function of individual thalamic nuclei in humans.

Indexed as

EthanolFetal Alcohol Spectrum DisordersPrenatal Exposure Delayed EffectsThalamusAnimalsFemaleHumansNeurogenesisPregnancyEthanolAlcoholAnimal modelDevelopmentEmbryonicFetalFunctionHumanImagingMorphologyPregnancyPrenatalStructureThalamus

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.