ArticleBrain research2015
Chronic intermittent ethanol induced axon and myelin degeneration is attenuated by calpain inhibition.
Article in Brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Novel neurotherapeutic targets for substance use disorders: Neuroplasticity, neuroinflammation, gasotransmitters and non-canonical organ systems.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Long-Term Excessive Alcohol Consumption Enhances Myelination in the Mouse Nucleus Accumbens.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Molecular and biochemical pathologies in human alcohol-related cerebellar white matter degeneration.Advances in drug and alcohol research · 2025Article
- Study on the protective effects and mechanisms of eleutherococcus senticosus on korsakoff syndrome.Frontiers in neuroscience · 2025Review
- Anti-Tumor Effect and Neurotoxicity of Ethanol Adjuvant Therapy after Surgery of a Soft Tissue Sarcoma.Current oncology (Toronto, Ont.) · 2023Article
- Cdk5 Promotes Mitochondrial Fission via Drp1 Phosphorylation at S616 in Chronic Ethanol Exposure-Induced Cognitive Impairment.Molecular neurobiology · 2022Article
- Impact of Alcohol Abuse on Susceptibility to Rare Neurodegenerative Diseases.Frontiers in molecular biosciences · 2021Review
- Chronic Ethanol Exposure Enhances Facial Stimulation-Evoked Mossy Fiber-Granule Cell Synaptic TransmissionFrontiers in systems neuroscience · 2021Article
- Bexarotene normalizes chemotherapy-induced myelin decompaction and reverses cognitive and sensorimotor deficits in mice.Acta neuropathologica communications · 2020Article
- Multi-modal imaging reveals differential brain volumetric, biochemical, and white matter fiber responsivity to repeated intermittent ethanol vapor exposure in male and female rats.Neuropharmacology · 2020Article
- Brain regional gene expression network analysis identifies unique interactions between chronic ethanol exposure and consumption.PloS one · 2020Article
- Alcohol intake and brain white matter in middle aged men: Microscopic and macroscopic differences.NeuroImage. Clinical · 2018Article
- Molecular Neuropathology of Astrocytes and Oligodendrocytes in Alcohol Use Disorders.Frontiers in molecular neuroscience · 2018Review
- Alcoholism and sexual dimorphism in the middle longitudinal fascicle: a pilot study.Brain imaging and behavior · 2017Article
- Genetic divergence in the transcriptional engram of chronic alcohol abuse: A laser-capture RNA-seq study of the mouse mesocorticolimbic system.Alcohol (Fayetteville, N.Y.) · 2017Article
- Calpain-mediated cleavage of collapsin response mediator protein-2 drives acute axonal degeneration.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic alcohol consumption causes multifaceted damage to the central nervous system (CNS), underlying mechanisms of which are gradually being unraveled. In our previous studies, activation of calpain, a calcium-activated neutral protease has been found to cause detrimental alterations in spinal motor neurons following ethanol (EtOH) exposure in vitro. However, it is not known whether calpain plays a pivotal role in chronic EtOH exposure-induced structural damage to CNS in vivo. To test the possible involvement of calpain in EtOH-associated neurodegenerative mechanisms the present investigation was conducted in a well-established mouse model of alcohol dependence - chronic intermittent EtOH (CIE) exposure and withdrawal. Our studies indicated significant loss of axonal proteins (neurofilament light and heavy, 50-60%), myelin proteins (myelin basic protein, 20-40% proteolipid protein, 25%) and enzyme (2', 3'-cyclic-nucleotide 3'-phosphodiesterase, 21-55%) following CIE in multiple regions of brain including hippocampus, corpus callosum, cerebellum, and importantly in spinal cord. These CIE-induced deleterious effects escalated after withdrawal in each CNS region tested. Increased expression and activity of calpain along with enhanced ratio of active calpain to calpastatin (sole endogenous inhibitor) was observed after withdrawal compared to EtOH exposure. Pharmacological inhibition of calpain with calpeptin (25 μg/kg) prior to each EtOH vapor inhalation significantly attenuated damage to axons and myelin as demonstrated by immuno-profiles of axonal and myelin proteins, and Luxol Fast Blue staining. Calpain inhibition significantly protected the ultrastructural integrity of axons and myelin compared to control as confirmed by electron microscopy. Together, these findings confirm CIE exposure and withdrawal induced structural alterations in axons and myelin, predominantly after withdrawal and corroborate calpain inhibition as a potential protective strategy against EtOH associated CNS degeneration.
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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.