Strain-Specific Differences in Perinatal Rodent Oligodendrocyte Lineage Progression and Its Correlation with Human

Dean, Justin M.; Moravec,; Grafe, Marjorie R.; Abend, Nicholas S.; Ren, Jennifer; Gong, Xun; Jj, Volpe; Fe, Jensen; Hohimer, A. Roger; Back, S. A.

doi:10.1159/000327242

Cited by 86 publications

(72 citation statements)

References 40 publications

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“…Rodents are altricial, with relatively immature brains at birth. Newborn rodents from P1 to P3 predominantly express preoligodendrocytes in the white matter, without evidence of myelination [78,79], consistent with the human fetus at 23-32 weeks. By P7 extensive oligodendrocyte maturation occurs in rodents, coinciding with the onset of early myelination, which is broadly consistent with late preterm to near term in human infants.…”

Section: Postnatal Infection/inflammation In Rodentsmentioning

confidence: 96%

A Critical Review of Models of Perinatal Infection

Dean¹,

Shi

Fleiss³

et al. 2015

Dev Neurosci

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One of the central, unanswered questions in perinatology is why preterm infants continue to have such poor long-term neurodevelopmental, cognitive and learning outcomes, even though severe brain injury is now rare. There is now strong clinical evidence that one factor underlying disability may be infection, as well as nonspecific inflammation, during fetal and early postnatal life. In this review, we examine the experimental evidence linking both acute and chronic infection/inflammation with perinatal brain injury and consider key experimental determinants, including the microglia response, relative brain and immune maturity and the pattern of exposure to infection. We highlight the importance of the origin and derivation of the bacterial cell wall component lipopolysaccharide. Such experimental paradigms are essential to determine the precise time course of the inflammatory reaction and to design targeted neuroprotective strategies to protect the perinatal brain from infection and inflammation.

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Section: Postnatal Infection/inflammation In Rodentsmentioning

confidence: 96%

A Critical Review of Models of Perinatal Infection

Dean¹,

Shi

Fleiss³

et al. 2015

Dev Neurosci

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“…Thus, the investigator can choose the appropriate developmental timing for the insult to be evaluated. Although in both humans and sheep, myelination begins prenatally, a notable difference is that myelinogensis progresses more rapidly in sheep [41] than in humans [43], which continues to progress for months after term birth [44]. By contrast, the rodent displays accelerated white matter maturation and myelination that occurs entirely postnatally [45].…”

Section: Advantages and Disadvantages Of The Fetal Sheep To Model Wmimentioning

confidence: 99%

“…By contrast, the rodent displays accelerated white matter maturation and myelination that occurs entirely postnatally [45]. In neonatal rats, for example, the progression from human preterm equivalent to near-term equivalent oligodendrocyte maturation occurs rapidly during the first 5 days after birth [44].…”

Section: Advantages and Disadvantages Of The Fetal Sheep To Model Wmimentioning

confidence: 99%

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

et al. 2012

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Despite advances in neonatal intensive care, survivors of premature birth remain highly susceptible to unique patterns of developmental brain injury that manifest as cerebral palsy and cognitive-learning disabilities. The developing brain is particularly susceptible to cerebral white matter injury related to hypoxia-ischemia. Cerebral white matter development in fetal sheep shares many anatomical and physiological similarities with humans. Thus, the fetal sheep has provided unique experimental access to the complex pathophysiological processes that contribute to injury to the human brain during successive periods in development. Recent refinements have resulted in models that replicate major features of acute and chronic human cerebral injury and have provided access to complex clinically relevant studies of cerebral blood flow and neuroimaging that are not feasible in smaller laboratory animals. Here, we focus on emerging insights and methodologies from studies in fetal sheep that have begun to define cellular and vascular factors that contribute to white matter injury. Recent advances include spatially defined measurements of cerebral blood flow in utero, the definition of cellular maturational factors that define the topography of injury and the application of high-field magnetic resonance imaging to define novel neuroimaging signatures for specific types of chronic white matter injury. Despite the higher costs and technical challenges of instrumented preterm fetal sheep models, they provide powerful access to clinically relevant studies that provide a more integrated analysis of the spectrum of insults that appear to contribute to cerebral injury in human preterm infants.

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“…As previously described, the majority of OLs at P6 in the periventricular white matter and cortex are O4 and O1 positive and not myelin basic protein (MBP) expressing (21,25). To test the hypothesis that NKCC1 was present on developing premyelinating OLs in white matter, immunostaining was done in the naive immature rat by double labeling for NKCC1 and the cell marker GalC (Figure 2a-c).…”

Section: Nkcc1 Is Expressed On Developing Ols and Neurons In The Immamentioning

confidence: 98%

“…The end of the first postnatal week (P5-7) in rodents is a period of heightened white matter vulnerability to HI compared to earlier or later ages (21,22). We have previously shown that this developmental stage is associated with higher levels of NKCC1 in cortical homogenates compared to adult (10).…”

Section: Nkcc1 Expression In the White Matter Peaks Early In The Perimentioning

confidence: 99%

Chloride cotransporter NKCC1 inhibitor bumetanide protects against white matter injury in a rodent model of periventricular leukomalacia

Jantzie

Park

et al. 2015

Pediatr Res

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Background: Periventricular leukomalacia (PVL) is a major form of preterm brain injury. Na + -K + -Cl − 1 cotransporter (NKCC1) expression on neurons and astrocytes is developmentally regulated and mediates Cl − reversal potential. We hypothesized that NKCC1 is highly expressed on oligodendrocytes (OLs) and increases vulnerability to hypoxia-ischemia (HI) mediated white matter injury, and that the NKCC1 inhibitor bumetanide would be protective in a rodent PVL model. Methods: Immunohistochemistry in Long-Evans rats and PLP-EGFP transgenic mice was used to establish cell-specific expression of NKCC1 in the immature rodent brain. HI was induced on postnatal day 6 (P6) in rats and the protective efficacy of bumetanide (0.3 mg/kg/i.p. q12h × 60 h) established. results: NKCC1 was expressed on OLs and subplate neurons through the first 2 postnatal weeks, peaking in white matter and the subplate between P3-7. Following HI, NKCC1 is expressed on OLs and neurons. Bumetanide treatment significantly attenuates myelin basic protein loss and neuronal degeneration 7 d post-HI. conclusion: Presence and relative overexpression of NKCC1 in rodent cerebral cortex coincides with a period of developmental vulnerability to HI white matter injury in the immature prenatal brain. The protective efficacy of bumetanide in this model of preterm brain injury suggests that Cl − transport is a factor in PVL and that its inhibition may have clinical application in premature human infants.

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Strain-Specific Differences in Perinatal Rodent Oligodendrocyte Lineage Progression and Its Correlation with Human

Cited by 86 publications

References 40 publications

A Critical Review of Models of Perinatal Infection

A Critical Review of Models of Perinatal Infection

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

Chloride cotransporter NKCC1 inhibitor bumetanide protects against white matter injury in a rodent model of periventricular leukomalacia

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