ArticleAlcoholism, clinical and experimental research2017
Chronic Ethanol During Adolescence Impacts Corticolimbic Dendritic Spines and Behavior.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry.Frontiers in neuroscience · 2022Pooled it
- Cued unpredictable intermittent access exacerbates loss of control over ethanol drinking.Neuropharmacology · 2026Article
- Developmental alcohol exposure: Impacts on medial prefrontal cortex morphology and the excitatory-inhibitory balance.Progress in neuro-psychopharmacology & biological psychiatry · 2026Review
- Cued unpredictable intermittent access exacerbates loss of control over ethanol drinking.bioRxiv : the preprint server for biology · 2026Article
- Prenatal antioxidant treatment suppresses maternal immune activation induced increases in alcohol self-administration in a sex-specific manner.Psychopharmacology · 2026Article
- mEnvironmental epigenetics · 2026Article
- Acetaldehyde-driven mRNA methylation and expression changes in ethanol-metabolizing enzyme genes.Epigenetics · 2025Article
- Chronic alcohol-induced brain states limit propagation of direct cortical stimulation.Scientific reports · 2025Article
- Individual differences in punished alcohol self-administration are unaltered by alcohol vapor exposure.Alcohol (Fayetteville, N.Y.) · 2025Observational
- Effect of chronic sleep restriction on ethanol preference and cortical structural plasticity.Neurobiology of sleep and circadian rhythms · 2025Article
- Effects of chronic ethanol exposure on dorsal medial striatal neurons receiving convergent inputs from the orbitofrontal cortex and basolateral amygdala.Neuropharmacology · 2025Article
- Chronic intermittent ethanol exposure-induced m6A modifications around mRNA stop codons of opioid receptor genes.Epigenetics · 2024Article
- Adolescent Alcohol Exposure Produces Sex-Specific Long-term Hyperalgesia via Changes in Central Amygdala Circuit Function.Biological psychiatry · 2024Article
- Adolescent intermittent ethanol exposure alters adult exploratory and affective behaviors, and cerebellar Grin2b expression in C57BL/6J mice.Drug and alcohol dependence · 2023Article
- Consequences of adolescent drug use.Translational psychiatry · 2023Review
- Sex- and age-specific effects on the development of addiction and compulsive-like drinking in rats.Biology of sex differences · 2023Article
- Chronic intermittent ethanol exposure differentially alters the excitability of neurons in the orbitofrontal cortex and basolateral amygdala that project to the dorsal striatum.Neuropharmacology · 2023Article
- Adolescent alcohol exposure reduces dopamine 1 receptor modulation of prelimbic neurons projecting to the nucleus accumbens and basolateral amygdala.Addiction neuroscience · 2022Article
- Adolescence alcohol exposure impairs fear extinction and alters medial prefrontal cortex plasticity.Neuropharmacology · 2022Article
- Alcohol Use Disorder: Neurobiology and Therapeutics.Biomedicines · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRisk for alcohol use disorders (AUDs) in adulthood is linked to alcohol drinking during adolescence, but understanding of the neural and behavioral consequences of alcohol exposure during adolescence remains incomplete. Here, we examined the neurobehavioral impact of adolescent chronic intermittent EtOH (CIE) vapor exposure in mice.
methodsC57BL/6J-background Thy1-EGFP mice were CIE-exposed during adolescence or adulthood and examined, as adults, for alterations in the density and morphology of dendritic spines in infralimbic (IL) cortex, prelimbic (PL) cortex, and basolateral amygdala (BLA). In parallel, adolescent- and adult-exposed C57BL/6J mice were tested as adults for 2-bottle EtOH drinking, sensitivity to EtOH intoxication (loss of righting reflex [LORR]), blood EtOH clearance, and measures of operant responding for food reward.
resultsCIE during adolescence decreased IL neuronal spine density and increased the head width of relatively wide-head IL and BLA spines, whereas CIE decreased head width of relatively narrow-head BLA spines. Adolescents had higher EtOH consumption prior to CIE than adults, while CIE during adulthood, but not adolescence, increased EtOH consumption relative to pre-CIE baseline. CIE produced a tolerance-like decrease in LORR sensitivity to EtOH challenge, irrespective of the age at which mice received CIE exposure. Mice exposed to CIE during adolescence, but not adulthood, required more sessions than AIR controls to reliably respond for food reward on a fixed-ratio (FR) 1, but not subsequent FR3, reinforcement schedule. On a progressive ratio reinforcement schedule, break point responding was higher in the adolescent- than the adult-exposed mice, regardless of CIE. Finally, footshock punishment markedly suppressed responding for reward in all groups.
conclusionsExposure to CIE during adolescence altered dendritic spine density and morphology in IL and BLA neurons, in parallel with a limited set of behavioral alterations. Together, these data add to growing evidence that key corticolimbic circuits are vulnerable to the effects of alcohol during adolescence, with lasting, potentially detrimental, consequences for behavior.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.