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

Intracranial hypocapnia is associated with parenchymal ischemia and worsened outcomes following stroke.

Journal of neurointerventional surgery·2026
Same author

Sex differences in proteomic response to ischemic stroke.

Biology of sex differences·2026
Same author

Expression of dementia biomarkers in Appalachian and non-Appalachian ELVO patients during thrombectomy.

Frontiers in neuroscience·2025
Same author

Role of interleukin-7 in acute large vessel occlusion stroke.

Journal of neurointerventional surgery·2025
Same author

Luminal Vascular Dysfunction Drives Rapid Blood Brain Barrier Injury in Hyperglycemic Stroke: Key Roles for Luminal Glycocalyx and Complement.

bioRxiv : the preprint server for biology·2025
Same author

Predictors and outcome metrics of futile recanalization in patients with acute ischemic stroke.

Journal of neurointerventional surgery·2025

Related Experiment Video

Updated: Feb 18, 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

Minocycline protects developing brain against ethanol-induced damage.

Xin Wang1, Kai Zhang1, Fanmuyi Yang1

  • 1Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.

Neuropharmacology
|November 18, 2017
PubMed
Summary

Minocycline protects developing brains from ethanol neurotoxicity by reducing neuroinflammation and microglial activation. This antibiotic therapy may offer a therapeutic strategy for fetal alcohol spectrum disorders (FASD).

Keywords:
ApoptosisDevelopmentFetal alcohol syndromeInflammationMicrogliaNeurodegeneration

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
Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice
09:50

Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice

Published on: April 24, 2013

12.2K

Related Experiment Videos

Last Updated: Feb 18, 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
Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice
09:50

Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice

Published on: April 24, 2013

12.2K

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Pharmacology

Background:

  • Fetal alcohol spectrum disorders (FASD), caused by prenatal ethanol exposure, are a leading cause of mental retardation.
  • Ethanol exposure during development leads to neuronal loss and neurobehavioral deficits, potentially involving neuroimmune activation.
  • Understanding ethanol's neurotoxic mechanisms is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the protective effects of minocycline against ethanol-induced neurotoxicity in a developing mouse brain model.
  • To determine if minocycline mitigates ethanol-induced neuroinflammation and microglial activation.
  • To explore the role of GSK3β in ethanol neurotoxicity and minocycline's effect on this pathway.

Main Methods:

  • Utilized a third-trimester equivalent mouse model of prenatal ethanol exposure.
  • Administered minocycline to assess its impact on ethanol-induced neuroapoptosis, microglial activation, and neuroinflammation.
  • Examined caspase-3 activation, pro- and anti-inflammatory cytokine expression, and GSK3β activation in vivo and in vitro (SIM-9 microglia cell line).
  • Conducted neuron-microglia co-culture experiments to evaluate minocycline's protective effects.

Main Results:

  • Ethanol exposure induced widespread neuroapoptosis, microglial activation, and neuroinflammation in C57BL/6 mice.
  • Minocycline significantly inhibited ethanol-induced caspase-3 activation, microglial activation, and pro-inflammatory cytokine expression.
  • Minocycline reversed ethanol's inhibition of anti-inflammatory cytokines and blocked ethanol-induced GSK3β activation.
  • In vitro studies confirmed minocycline's inhibition of pro-inflammatory cytokines and GSK3β activation in microglia.
  • Minocycline protected neurons from ethanol-induced death in co-cultures.

Conclusions:

  • Minocycline effectively ameliorates ethanol neurotoxicity in the developing brain by inhibiting microglial activation and neuroinflammation.
  • The protective mechanism involves the modulation of GSK3β signaling, a key mediator of neuroinflammation.
  • Minocycline shows promise as a therapeutic agent for mitigating the neurodevelopmental consequences of prenatal ethanol exposure.