Formation of Myelin in the Central Nervous System of Mice and Rats, as Studied With the Electron Microscope

Abstract

Myelin formation and its relation to the neuroglia has been a problem of continuing interest to neurocytologists since the early work of Jastrowitz (1), Boll (2), and Wlassak (3). It was not until 1928, however, that del Rio-Hortega (4) ascribed to the oligodendroglia a definite role in the process of myelinization. Since then other workers (5, 6) have supported del Rio-Hortega's thesis, although Alpers and Haymaker (6) proposed that not only the oligoglia but the astroglia are in some way implicated in the process of myelinization.Schmitt, Bear, and Palmer (7) by x-ray diffraction obtained a pattern suggesting that tile myelin of peripheral nerves is arranged as a laminated structure. This pattern has been corroborated by the electron microscopic observations of Fern~ndez-Mor~n (8), Sj/3strand (9), Geren and Raskind (10), and Robertson (11). With the resolution afforded by the electron microscope and the now available methods of fixation and thin sectioning, the mechanism of myelinization is in need of reinvestigation. Geren (12) has shown that the laminae of the myelinated sheath of a peripheral nerve are helically disposed continuations of the plasma membrane of the contiguous Schwann cell.The myelinated sheath in the central nervous system also is comprised of closely arranged lamellae and Luse (14)). The source of these membranes in the central nervous system is not obvious, for not one but many cells may abut upon a single axon. In an attempt to determine the origin of the lamellated membranes within the myelinated sheaths of axons in the central nervous system, the brains and spinal cords of young mice and rats were examined during the period of myelinization. Materials and MethodsMice and rats were killed at 1, 3, 5, and 17 days after birth. Small pieces of spinal cord, medulla, and occipital cortex were rapidly removed from decapitated animals and immedi-* This investigation has been aided in part by grants (C-2755 and B-425) from the United States

Jun�n virus encephalitis in mice: Its inhibition by antithymocyte serum

“…Myelin studies were rendered difficult because in mice myelination is not completed until almost the 17th day after birth (13). However from day 10 till death, generally on day 14, some evidences of demyelination surrounding perivascular cuffs could be observed.…”

CNS myelin sheath is stochastically built by homotypic fusion of myelin membranes within the bounds of an oligodendrocyte process

“…The large body of work on this topic has, insightfully, been reviewed by Bunge (Bunge, 1968), who grouped the prevailing ideas into three concepts. Concept 1 (Luse, 1956) -derived from studies of mouse and rat brains and spinal cord -sustained that CNS myelin originates from a patchwork assembly of many different glial processes arising from one or more glial cells. Concept 2 referred to the daring hypothesis -originated from work on kitten brain and spinal cord -that the myelin sheath was formed by the coalescence of intracytoplasmic membranes rather than from the plasma membrane (De Robertis et al, 1958).…”

Maternal Alcohol Consumption Increases Sphingosine Levels in the Brains of Progeny Mice

“…There are also reports examining brain development in mice [16][17][18][19][20][21]. In the present study, we chose the mouse as FAS model for study of sphingolipid metabolism during CNS development because: (1) there is a long history of studies of brain development and myelination in mice [22][23][24][25][26][27] (2) mice are more sensitive to alcoholinduced dysmorphology than rats [28,29]; (3) genetic mouse models, including jimpy, quaking, shiverer and twitcher mutants, have been extensively studied as models for human dysmyelinating disorders [30]; and, (4) the technology for knocking out a specific gene that is particularly well suited for elucidating the mechanisms of developmental neurobiology and human brain disorders is carried out mainly in mice [31][32][33][34][35][36][37]. With the availability of suitable knockout mutants (e.g., NMDA receptor/GABA receptor knockout), mice are the most valuable model for studying the mechanism of alcohol-mediated perturbation of CNS development and myelination.…”