Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption

Okamoto, Hanayo; Miki, Takanori; Lee, Kyoung-Youl; Yokoyama, Toshifumi; Kuma, Hiromi; Wang, Zhiyu; He, Gu; Liu, Hongpeng; Matsumoto, Yoshiki; Satriotomo, Irawan; Bedi, K. S.; Nakamura, Yu; Takeuchi, Yoshiki

doi:10.1016/j.neulet.2006.07.023

Cited by 26 publications

(10 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…First, hippocampus is a site of major emphasis as it has been previously reported to be a predominant region of impairment leading to alcohol-associated dysfunctions (Vilpoux et al, 2009). Loss of myelin proteins has been previously found in hippocampus (Alfonso-Loeches et al, 2012; Lee et al, 2010; Okamoto et al, 2006). Alterations in myelin and axonal integrity in hippocampus may underlie cognitive deficits as previously reported (Dutta et al, 2011; Dutta et al, 2013).…”

Section: Discussionmentioning

confidence: 83%

Chronic intermittent ethanol induced axon and myelin degeneration is attenuated by calpain inhibition

et al. 2015

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 83%

Chronic intermittent ethanol induced axon and myelin degeneration is attenuated by calpain inhibition

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Alcohol‐related brain effects may also be due to an upregulation of inflammatory mediators (e.g., COX‐2 and inducible nitric oxide synthase [iNOS]) that ultimately lead to neural cell death or injury (Blanco et al., 2005; Pascual et al., 2007; Valles et al., 2004). Alternatively, the observed reduced PFC volumes among the females may have been driven exclusively by white matter pathology (Harper et al., 1990; Okamoto et al., 2006). Larger studies examining PFC morphometry among adolescents with AUD are necessary to determine whether the observed volume abnormalities are primarily due to white or gray matter pathology and to assess whether these structural differences are associated with altered cognitive functioning.…”

Section: Discussionmentioning

confidence: 99%

Prefrontal Cortex Volumes in Adolescents With Alcohol Use Disorders: Unique Gender Effects

Medina

McQueeny

Nagel

et al. 2008

Alcoholism Clin & Exp Res

301

252

View full text Add to dashboard Cite

Background: Adolescents with alcohol use disorders (AUD) have shown smaller prefrontal cortex (PFC) volumes compared with healthy controls; however, differences may have been due to comorbid disorders. This study examined PFC volumes in male and female adolescents with AUD who did not meet criteria for comorbid mood or attention disorders.Methods: Participants were adolescents aged 15 to 17 who met criteria for AUD (n = 14), and demographically similar healthy controls (n = 17). Exclusions included any history of a psychiatric or neurologic disorder other than AUD or conduct disorder. Magnetic resonance imaging scans occurred after at least 5 days of abstinence from alcohol or drugs. Overall PFC volumes and white matter PFC volumes were compared between groups.Results: After controlling for conduct disorder, gender, and intracranial volume, AUD teens demonstrated marginally smaller anterior ventral PFC volumes (p = 0.09) than controls, and significant interactions between group and gender were observed (p < 0.001 to p < 0.03). Compared with same-gender controls, females with AUD demonstrated smaller PFC volumes, while males with AUD had larger PFC volumes. The same pattern was observed for PFC white matter volumes.Conclusions: Consistent with adult literature, alcohol use during adolescence is associated with prefrontal volume abnormalities, including white matter differences. However, adolescents with AUD demonstrated gender-specific morphometric patterns. Thus, it is possible that gender may moderate the impact of adolescent alcohol use on prefrontal neurodevelopment, and the neurodevelopmental trajectories of heavy drinking boys and girls should be evaluated separately in longitudinal studies.

show abstract

“…Cannabis-induced alterations in myelin proteolipid protein could also affect the expression of this gene, particularly with long-term exposure (Grigorenko et al, 2002). Down-regulation of myelin-related genes (Lewohl et al, 2000; Mayfield et al, 2002) and deficits in oligodendrocyte myelin glycoprotein (Okamoto et al, 2006) found in chronic alcoholism may further interact with altered processes associated with cannabis exposure. Focal areas of fiber disintegrity, as suggested by the current study, may result from any of these neurodevelopmental processes.…”

Section: Discussionmentioning

confidence: 99%

Altered white matter microstructure in adolescent substance users

Bava

Frank

McQueeny

et al. 2009

Psychiatry Research: Neuroimaging

161

163

View full text Add to dashboard Cite

Chronic marijuana use during adolescence is frequently comorbid with heavy alcohol consumption and associated with CNS alterations, yet the influence of early cannabis and alcohol use on microstructural white matter integrity is unclear. Building on evidence that cannabinoid receptors are present in myelin precursors and affect glial cell processing, and that excessive ethanol exposure is associated with persistently impaired myelination, we used diffusion tensor imaging (DTI) to characterize white matter integrity in heavy substance using and non-using adolescents. We evaluated 36 marijuana and alcohol-using (MJ+ALC) adolescents (ages 16-19) and 36 demographically similar non-using controls with DTI. Diffusion parameters fractional anisotropy (FA) and mean diffusivity (MD) were subjected to whole-brain voxelwise group comparisons using tract-based spatial statistics (Smith et al., 2006). MJ+ALC teens had significantly lower FA than controls in 10 regions, including left superior longitudinal fasciculus (SLF), left postcentral gyrus, bilateral crus cerebri, and inferior frontal and temporal white matter tracts. These diminutions occurred in the context of increased FA in right occipital, internal capsule, and SLF regions. Changes in MD were less distributed, but increased MD was evident in the right occipital lobe, whereas the left inferior longitudinal fasciculus showed lower MD in MJ+ALC users. Findings suggest that fronto-parietal circuitry may be particularly impacted in adolescent users of the most prevalent intoxicants: marijuana and alcohol. Disruptions to white matter in this young group could indicate aberrant axonal and myelin maturation with resultant compromise of fiber integrity. Findings of increased anisotropic diffusion in alternate brain regions suggests possible neuroadaptive processes and can be examined in future studies of connectivity to determine how aberrancies in specific tracts might influence efficient cognitive processing.

show abstract

Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption

Cited by 26 publications

References 23 publications

Chronic intermittent ethanol induced axon and myelin degeneration is attenuated by calpain inhibition

Chronic intermittent ethanol induced axon and myelin degeneration is attenuated by calpain inhibition

Prefrontal Cortex Volumes in Adolescents With Alcohol Use Disorders: Unique Gender Effects

Altered white matter microstructure in adolescent substance users

Contact Info

Product

Resources

About