Sexual dimorphism in the white matter of rodents

Cerghet, Mirela; Skoff, Robert P.; Swamydas, Muthulekha; Bessert, Denise

doi:10.1016/j.jns.2009.06.039

Cited by 61 publications

(51 citation statements)

References 65 publications

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“…Sex-separate analysis of neurophysiological data due to the variance in vulnerability between males and females to the constellation of teratogenic effects induced by perinatal EtOH is increasingly recognized as important (Paolozza et al 2014; Tesche et al 2015). Sexual dimorphism of oligodendrocytes and myelin gene expression in the corpus callosum has been consistently observed in the brains of normally developing rodents (Cerghet et al 2009), but the sex-specific effects of prenatal EtOH exposure on oligodendrocyte cells has not been comprehensively explored (Wilhelm and Guizzetti 2015). Recent research supports the hypothesis that sex-specific effects in white matter regions exist in models of FASD.…”

Section: Discussionmentioning

confidence: 99%

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorder

Newville

Valenzuela

et al. 2017

Glia

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Alcohol exposure during central nervous system (CNS) development can lead to fetal alcohol spectrum disorder (FASD). Human imaging studies have revealed significant white matter (WM) abnormalities linked to cognitive impairment in children with FASD, however the underlying mechanisms remain unknown. Here, we evaluated both the acute and long-term impacts of alcohol exposure on oligodendrocyte number and WM integrity in a third trimester-equivalent mouse model of FASD, in which mouse pups were exposed to alcohol during the first two weeks of postnatal development. Our results demonstrate a 58% decrease in the number of mature oligodendrocytes (OLs) and a 75% decrease in the number of proliferating oligodendrocyte progenitor cells (OPCs) within the corpus callosum of alcohol-exposed mice at postnatal day 16 (P16). Interestingly, neither mature OLs nor OPCs derived from the postnatal subventricular zone (SVZ) were numerically affected by alcohol exposure, indicating heterogeneity in susceptibility based on OL ontogenetic origin. Although mature OL and proliferating OPC numbers recovered by postnatal day 50 (P50), abnormalities in myelin protein expression and microstructure within the corpus callosum of alcohol-exposed subjects persisted, as assessed by western immunoblotting of myelin basic protein (MBP; decreased expression) and MRI diffusion tensor imaging (DTI; decreased fractional anisotropy). These results indicate that third trimester-equivalent alcohol exposure leads to an acute, albeit recoverable, decrease in OL lineage cell numbers, accompanied by enduring WM injury. Additionally, our finding of heterogeneity in alcohol susceptibility based on the developmental origin of OLs may have therapeutic implications in FASD and other disorders of WM development.

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Section: Discussionmentioning

confidence: 99%

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorder

Newville

Valenzuela

et al. 2017

Glia

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show abstract

“…In this regard, it is important to point out that the present findings are reported as the pooled results from an equal number of male and female pups, as we failed to detect any significant sex-dependent differences. However, previous studies have reported sex related variations in opioid responses (reviewed by Bodnar and Kest [48]) as well as sexual dimorphism in rodent oligodendrocytes and white matter (reviewed by Cerghet et al [49]). Therefore, we cannot discard the possibility that such related differences may manifest at later stages of development.…”

Section: Discussionmentioning

confidence: 99%

The Opioid System and Brain Development: Effects of Methadone on the Oligodendrocyte Lineage and the Early Stages of Myelination

Vestal-Laborde

Eschenroeder²,

Bigbee³

et al. 2014

Dev Neurosci

116

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Oligodendrocytes express opioid receptors throughout development, but the role of the opioid system in myelination remains poorly understood. This is a significant problem as opioid use and abuse continue to increase in two particular populations: pregnant addicts (in whom drug effects could target early myelination in the fetus and newborn) and adolescents and young adults (in whom late myelination of ‘higher-order' regions takes place). Maintenance treatments for opioid addicts include the long-lasting opioids methadone and buprenorphine. Similar to our previous findings on the effects of buprenorphine, we have now found that early myelination in the developing rat brain is also altered by perinatal exposure to therapeutic doses of methadone. Pups exposed to this drug exhibited elevated brain levels of the 4 major splicing variants of myelin basic protein, myelin proteolipid protein, and myelin-oligodendrocyte glycoprotein. Consistent with the enrichment and function of these proteins in mature myelin, analysis of the corpus callosum in these young animals also indicated an elevated number of axons with already highly compacted myelin sheaths. Moreover, studies in cultured cells showed that methadone exerts direct effects at specific stages of the oligodendrocyte lineage, stimulating the proliferation of progenitor cells while on the other hand accelerating the maturation of the more differentiated but still immature preoligodendrocytes. While the long-term effects of these observations remain unknown, accelerated or increased oligodendrocyte maturation and myelination could both disrupt the complex sequence of synchronized events leading to normal connectivity in the developing brain. Together with our previous observations on the effects of buprenorphine, the present findings further underscore a crucial function of the endogenous opioid system in the control of oligodendrocyte development and the timing of myelination. Interference with these regulatory systems by opioid use or maintenance treatments could disrupt the normal process of brain maturation at critical stages of myelin formation.

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“…This effect is equally observed in males and females (Markham et al, 2009), although several measures showed robust sex differences in naive animals, with males having larger callosal regions and more area occupied by myelinated axons than females (Yates and Juraska, 2007;Markham et al, 2009). In rats, there are links between hormones and oligodendrocytes, suggesting a role for hormones in shaping white matter fiber tracts in these animals (Cerghet et al, 2009).…”

Section: Developmental and Activitydependent Changes In Visual Callosmentioning

confidence: 99%

Visual callosal connections: role in visual processing in health and disease

Bocci¹,

Pietrasanta²,

Cerri³

et al. 2014

Reviews in the Neurosciences

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Sexual dimorphism in the white matter of rodents

Cited by 61 publications

References 65 publications

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorder

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorder

The Opioid System and Brain Development: Effects of Methadone on the Oligodendrocyte Lineage and the Early Stages of Myelination

Visual callosal connections: role in visual processing in health and disease

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