Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Disrupted maternal care alters neural-microglia interactions in the primate paralaminar (PL) nucleus of the amygdala.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026
Same author

Epicardial Contributions to Fibro-Inflammatory Signaling in a Pkp2-Deficient Arrhythmogenic Cardiomyopathy Model.

Circulation. Heart failure·2026
Same author

Characterization of Genetic Etiologic Factors for Pediatric Acute Lymphoblastic Leukemia in Large Childhood Cancer Survivorship Cohorts.

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology·2026
Same author

Early Postnatal Ethanol Exposure Has Long-Term Behavioral Consequences in Female Mice.

Cells·2026
Same author

Dynamics of neutrophilia at the neurovascular unit arising from repeated pulmonary inflammation.

Journal of neuroinflammation·2026
Same author

Disrupted maternal care alters neural-microglia interactions in the primate paralaminar (PL) nucleus of the amygdala.

bioRxiv : the preprint server for biology·2026
Same journal

Hippocampal C5a-C5aR1 axis drives age-related memory decline via collapsing synaptic chloride homeostasis.

Brain, behavior, and immunity·2026
Same journal

Bifidobacterium bifidum TMC3115-RAW264.7 cell conditioned mediums promote the synaptic development of primary hippocampal neuron via activating IL-6/JAK2/STAT3 signaling pathway.

Brain, behavior, and immunity·2026
Same journal

T cells contribute to approaching positive but potentially risky stimuli through medial prefrontal cortex immune modulation.

Brain, behavior, and immunity·2026
Same journal

Insulin modulates mPFC gene expression and emotional behavior in a sex-specific manner following fetal growth restriction.

Brain, behavior, and immunity·2026
Same journal

Activation of the cGAS-STING pathway contributes to cancer-related fatigue in a murine model of head and neck cancer.

Brain, behavior, and immunity·2026
Same journal

Monocyte abundance and glycolytic reprogramming associate with motivational impairment in depression.

Brain, behavior, and immunity·2026
See all related articles

Related Experiment Video

Updated: Feb 22, 2026

Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development
15:27

Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development

Published on: July 13, 2014

15.2K

Developmental alcohol exposure impairs synaptic plasticity without overtly altering microglial function in mouse

Elissa L Wong1, Nina M Lutz2, Victoria A Hogan2

  • 1Dept. of Environmental Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.

Brain, Behavior, and Immunity
|September 18, 2017
PubMed
Summary
This summary is machine-generated.

Early ethanol exposure impairs brain plasticity in developing mice, leading to lasting deficits in visual processing. This occurs independently of microglial activation or dysfunction, highlighting broader impacts on neural development.

Keywords:
EthanolFetal alcohol spectrum disorderIn vivo two-photon microscopyMicrogliaMouse modelSynaptic plasticityTranscriptome

More Related Videos

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
19:57

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

Published on: August 5, 2017

8.9K
Wheel Running and Environmental Complexity as a Therapeutic Intervention in an Animal Model of FASD
06:09

Wheel Running and Environmental Complexity as a Therapeutic Intervention in an Animal Model of FASD

Published on: February 2, 2017

7.2K

Related Experiment Videos

Last Updated: Feb 22, 2026

Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development
15:27

Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development

Published on: July 13, 2014

15.2K
The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
19:57

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

Published on: August 5, 2017

8.9K
Wheel Running and Environmental Complexity as a Therapeutic Intervention in an Animal Model of FASD
06:09

Wheel Running and Environmental Complexity as a Therapeutic Intervention in an Animal Model of FASD

Published on: February 2, 2017

7.2K

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Neuroimmunology

Background:

  • Fetal alcohol spectrum disorder (FASD) from gestational ethanol (EtOH) exposure causes lifelong mental disability with no cure.
  • EtOH's effects on brain development and resulting sensory/cognitive deficits are not fully understood.
  • Microglia are crucial for neural development and plasticity, and can react to EtOH.

Purpose of the Study:

  • To investigate if early EtOH exposure permanently alters microglial function, leading to deficits in experience-dependent plasticity.
  • To examine the impact of developmental EtOH exposure on synaptic plasticity in the visual cortex.
  • To determine if microglial dysfunction underlies EtOH-induced neurodevelopmental deficits.

Main Methods:

  • Utilized a mouse model of high-binge EtOH exposure during early development (postnatal days 4-9).
  • Assessed experience-dependent plasticity using a monocular deprivation paradigm in the visual cortex.
  • Analyzed microglial morphology, dynamics, and transcriptome using microscopy, FACS, and RNA-seq.

Main Results:

  • Early EtOH exposure induced deficits in visually driven experience-dependent plasticity.
  • No evidence of microglial dysfunction, activation, or altered transcriptome was found in early adolescence.
  • No EtOH-induced neuronal cell death was observed in the visual cortex.

Conclusions:

  • Developmental EtOH exposure impairs experience-dependent synaptic plasticity in the visual cortex.
  • This plasticity deficit is independent of microglial activation or functional changes.
  • Neural plasticity can be impaired by developmental ethanol exposure even without microglial activation.