Progress of myelination in the human fetal spinal nerve roots, spinal cord and brainstem with myelin basic protein immunohistochemistry

Tanaka, Soichiro; Mito, Takashi; Takashima, Sachio

doi:10.1016/0378-3782(94)01608-r

Cited by 51 publications

(37 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1,2 Elevated MPF in the brain stem observed in the second trimester agrees with the earliest myelination onset (around the 20th gestational week) in certain fiber tracts, such as the medial lemniscus and medial longitudinal fasciculus. 1,23,24 A relatively high MPF and its correlation with GA in the thalamus are also in concordance with early myelination of this structure commencing at the 25th week. 25 While the myelin content provides the main determinant of the MPF in WM according to our results and other studies, [6][7][8][9][10] subtle effects of other tissue properties on this parameter are also discernible.…”

Section: Discussionmentioning

confidence: 51%

Quantitative Assessment of Normal Fetal Brain Myelination Using Fast Macromolecular Proton Fraction Mapping

Yarnykh

Prihod'ko

Савелов

et al. 2018

AJNR Am J Neuroradiol

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 51%

Quantitative Assessment of Normal Fetal Brain Myelination Using Fast Macromolecular Proton Fraction Mapping

Yarnykh

Prihod'ko

Савелов

et al. 2018

AJNR Am J Neuroradiol

View full text Add to dashboard Cite

show abstract

“…In humans, myelination initiates during the second trimester (Tanaka et al 1995), although the exact time table may vary from one region of the nervous system to another. In this study, claudin-1, claudin-3, occludin, and ZO-1 antibodies showed punctate labeling with mesaxon-like profiles in the second trimester, and occasional Schmidt-Lanterman incisures and paranodal regions can be distinguished during the third trimester, indicating the formation of immature TJs and the initiation of at least a minimum of myelin compaction by 37 weeks of gestation.…”

Section: Discussionmentioning

confidence: 99%

Tight Junction Proteins in Human Schwann Cell Autotypic Junctions

Alanne

Pummi

Heape

et al. 2009

J Histochem Cytochem.

View full text Add to dashboard Cite

(AMH) S U M M A R Y Tight junctions (TJs) form physical barriers in various tissues and regulate paracellular transport of ions, water, and molecules. Myelinating Schwann cells form highly organized structures, including compact myelin, nodes of Ranvier, paranodal regions, Schmidt-Lanterman incisures, periaxonal cytoplasmic collars, and mesaxons. Autotypic TJs are formed in non-compacted myelin compartments between adjacent membrane lamellae of the same Schwann cell. Using indirect immunofluorescence and RT-PCR, we analyzed the expression of adherens junction (E-cadherin) and TJ [claudins, zonula occludens (ZO)-1, occludin] components in human peripheral nerve endoneurium, showing clear differences with published rodent profiles. Adult nerve paranodal regions contained E-cadherin, claudin-1, claudin-2, and ZO-1. Schmidt-Lanterman incisures contained E-cadherin, claudin-1, claudin-2, claudin-3, claudin-5, ZO-1, and occludin. Mesaxons contained E-cadherin, claudin-1, claudin-2, claudin-3, ZO-1, and occludin. None of the proteins studied were associated with nodal inter-Schwann cell junctions. Fetal nerve expression of claudin-1, claudin-3, ZO-1, and occludin was predominantly punctate, with a mesaxonal labeling pattern, but paranodal (ZO-1, claudin-3) and Schmidt-Lanterman incisure (claudins-1 and -3) expression profiles typical of compact myelin were visible by gestational week 37. The clear differences observed between human and published rodent nerve profiles emphasize the importance of human studies when translating the results of animal models to human diseases. PERIPHERAL AXONS are isolated from the surrounding non-nervous tissues by a triple layer of collagen-based connective tissue, including the outermost epineurial layer, that surrounds the whole nerve, the perineurium, which surrounds nerve fascicles, and the innermost endoneurial layer that surrounds individual nerve fibers, and by a Schwann cell sheath. In adults, the Schwann cells form either a myelin sheath or an amyelin sheath. Myelinating Schwann cells wrap around the axon, forming highly organized, compacted, and noncompacted, multilamellar membrane structures. The non-compact structures include the paranodal loop regions, the Schmidt-Lanterman incisures, the periaxonal cytoplasmic collar, and the inner and outer mesaxons. At the nodes of Ranvier, interdigitations of the plasma membranes of adjacent Schwann cells assure the continuity of the Schwann cell sheath along the whole length of the axon, while a continuous, Schwann cell-derived basal lamina forms a permeable boundary between the endoneurial connective tissue layer and the Schwann cell myelin sheath (Thomas 1963).Perineurial cells of the perineurium form a selective diffusion barrier between the endoneurium and the epineurium (Thomas 1963;Jaakkola et al. 1993;Pummi et al. 2004), and we have previously shown that the tight junction (TJ) proteins zonula occludens (ZO)-1, occludin, claudin-1, and claudin-3 all contribute to the formation of this perineurial diffusion barrier in human Cor...

show abstract

“…Longer-term outcomes may be suggested by evaluating myelination in neonatal brain as an important index of normal maturation and development (27). We concentrated on the corpus callosum and cingulum for preservation and recovery of white matter after HI injury since decrease in the size of the corpus callosum has been shown to adversely affect the motor co-ordination in the preterm neonates at a later age (28).…”

Section: Discussionmentioning

confidence: 99%

Combination of Systemic Hypothermia and N-acetylcysteine Attenuates Hypoxic-Ischemic Brain Injury in Neonatal Rats

et al. 2006

View full text Add to dashboard Cite

Hypoxic ischemic (HI) injury in neonates may have devastating, long-term consequences. Recently completed clinical trials in HI neonates indicate that hypothermia within 6 h of birth results in modest improvement in the combined outcome of death or severe disability. The aim of this study was to investigate the effects of combining hypothermia and N-acetylcysteine (NAC) on brain injury, neonatal reflexes and myelination after neonatal HI. Sevenday-old rats were subjected to right common carotid artery ligation and hypoxia (8% oxygen) for 2 h. Systemic hypothermia (30 ϩ 0.5°C) was induced immediately after the period of HI and was maintained for 2 h. NAC (50 mg/kg) was administered by intraperitoneal injection daily until sacrifice. Brain infarct volumes were significantly reduced at 48 h post-HI in the hypothermia plus NAC group (21.5 Ϯ 3.84 mm3) compared with vehicle (240.85 Ϯ 4.08 mm 3 ). Neonatal reflexes were also significantly improved by combination therapy at days 1 and 7. There was a significant loss of right hemispheric brain volume in the untreated group at 2 and 4 wk after HI insult. Brain volumes were preserved in hypothermia plus NAC group and were not significantly different when compared with the sham group. Similarly, increased myelin expression was seen in brain sections from hypothermia plus NAC group, when stained for Luxol Fast Blue (LFB), Myelin Basic Protein (MBP) and Proteolipid protein (PLP). These results indicate that hypothermia plus NAC combination therapy improves infarct volume, myelin expression and functional outcomes after focal HI injury. H ypoxic ischemic (HI) injury in neonates occurs in termneonates at a frequency of 1-4 per 1,000 live births (1) and may result in reduced potential for motor and cognitive development (2,3). Hypothermia improves survival and neurologic outcomes in neonatal animal models of severe HI injury (4 -7), and in recently completed clinical trials of HI neonates when instituted within 6 h of birth (8 -11). Animal data shows that initiation of hypothermia between 6 and 12 h after HI reduces cerebral injury (12,13), perhaps moderating secondary injury cascades during a time when cellular recovery is still possible. However, some inflammatory mediators are merely delayed by hypothermia treatment (14), indicating that hypothermia may be most helpful in extending the therapeutic window after HI injury.Therefore, the combination of hypothermia with other pharmacologic interventions may allow for significant improvements in outcome, which are not possible when the therapies are used separately. There have been limited reports of hypothermia treatment with other pharmacologic interventions. Systemic hypothermia and a pan-caspase inhibitor, bocaspartyl-(OMe)-fluoromethyl-ketone (BAF), produced a strong protective effect against neuronal cell damage in the ipsilateral hippocampal CA1 region of the developing rat brain, along with a reduction in caspase-3 activity (15). The combination of MK-801 and hypothermia also protected animals against HI injury ...

show abstract

Progress of myelination in the human fetal spinal nerve roots, spinal cord and brainstem with myelin basic protein immunohistochemistry

Cited by 51 publications

References 16 publications

Quantitative Assessment of Normal Fetal Brain Myelination Using Fast Macromolecular Proton Fraction Mapping

Quantitative Assessment of Normal Fetal Brain Myelination Using Fast Macromolecular Proton Fraction Mapping

Tight Junction Proteins in Human Schwann Cell Autotypic Junctions

Combination of Systemic Hypothermia and N-acetylcysteine Attenuates Hypoxic-Ischemic Brain Injury in Neonatal Rats

Contact Info

Product

Resources

About