Search results for "Binge ethanol treatment"

showing 4 items of 4 documents

TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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Involvement of TLR4 in the long-term epigenetic changes, rewarding and anxiety effects induced by intermittent ethanol treatment in adolescence

2016

Studies in humans and experimental animals have demonstrated the vulnerability of the adolescent brain to actions of ethanol and the long-term consequences of binge drinking, including the behavioral and cognitive deficits that result from alcohol neurotoxicity, and increased risk to alcohol abuse and dependence. Although the mechanisms that participate in these effects are largely unknown, we have shown that ethanol by activating innate immune receptors, toll-like receptor 4 (TLR4), induces neuroinflammation, impairs myelin proteins and causes cognitive dysfunctions in adolescent mice. Since neuroimmune signaling is also involved in alcohol abuse, the aim of this study was to assess whethe…

Male0301 basic medicineEpigenetic changesmedia_common.quotation_subjectImmunologyRewarding effectsAlcohol abuseBinge drinkingAnxietyBinge DrinkingEpigenesis GeneticMice03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineRewardNeuroimmune systemmedicineAnimalsTLR4Neuroinflammationmedia_commonMice KnockoutEthanolBinge ethanol treatmentEndocrine and Autonomic SystemsAddictionAge FactorsNeurotoxicityBrainAnxiety-like behaviormedicine.diseaseEthanol preferencePrelimbic medial prefrontal cortexAdolescenceMice Inbred C57BLToll-Like Receptor 4Alcoholism030104 developmental biologySynaptic plasticityFemaleCognition DisordersPsychologyNeuroscienceMyelin Proteins030217 neurology & neurosurgeryFOSBBrain, Behavior, and Immunity
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Role of mTOR-regulated autophagy in spine pruning defects and memory impairments induced by binge-like ethanol treatment in adolescent mice.

2021

Abstract Adolescence is a brain maturation developmental period during which remodeling and changes in synaptic plasticity and neural connectivity take place in some brain regions. Different mechanism participates in adolescent brain maturation, including autophagy that plays a role in synaptic development and plasticity. Alcohol is a neurotoxic compound and its abuse in adolescence induces neuroinflammation, synaptic and myelin alterations, neural damage and behavioral impairments. Changes in synaptic plasticity and its regulation by mTOR have also been suggested to play a role in the behavioral dysfunction of binge ethanol drinking in adolescence. Therefore, by considering the critical ro…

MaleautophagyDendritic spineSynaptic pruningPeriod (gene)synaptic pruningBiologyPathology and Forensic MedicineBinge Drinkingbinge ethanol treatmentMyelinMicemedicineAnimalsPI3K/AKT/mTOR pathwayNeuroinflammationResearch Articlescognitive functionMemory DisordersNeuronal PlasticityGeneral NeuroscienceTOR Serine-Threonine KinasesAutophagyBraindendritic spinesMice Inbred C57BLmedicine.anatomical_structureSynaptic plasticitymTORFemaleadolescenceNeurology (clinical)NeuroscienceResearch ArticleBrain pathology (Zurich, Switzerland)
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Binge-like ethanol treatment in adolescence impairs autophagy and hinders synaptic maturation: Role of TLR4.

2018

Abstract Adolescence is a developmental period of brain maturation in which remodeling and changes in synaptic plasticity and neural connectivity take place in some brain regions. A different mechanism participates in adolescent brain maturation, including autophagy processes that play a role in synaptic development and plasticity. Alcohol is a neurotoxic compound whose abuse in adolescence causes TLR4 response activation by triggering neuroinflammation, neural damage and behavioral alterations. However, the potential participation of autophagy in long-term neurochemical and cognitive dysfunctions induced by binge ethanol drinking in adolescence is uncertain. We therefore evaluated whether …

0301 basic medicineNeurogenesisImmune receptorBiologyBinge Drinking03 medical and health sciencesMice0302 clinical medicineNeurochemicalAutophagyAnimalsTLR4PI3K/AKT/mTOR pathwayNeuroinflammationMice KnockoutBinge ethanol treatmentEthanolGeneral NeuroscienceAutophagyAge FactorsAdolescenceMice Inbred C57BLToll-Like Receptor 4030104 developmental biologyStructural synaptic plasticitySynaptic plasticitySynapsesExcitatory postsynaptic potentialTLR4FemaleNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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