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Oxydative phosphorylation in sciatic nerve myelin and its impairment in a model of dysmyelinating peripheral neuropathy
Author(s) -
Ravera Silvia,
Nobbio Lucilla,
Visigalli Davide,
Bartolucci Martina,
Calzia Daniela,
Fiorese Fulvia,
Mancardi Gianluigi,
Sche Angelo,
Morelli Alessandro,
Panfoli Isabella
Publication year - 2013
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.12253
Subject(s) - myelin , sciatic nerve , oxidative phosphorylation , mitochondrion , schwann cell , peripheral nervous system , neuroregeneration , biology , microbiology and biotechnology , chemistry , peripheral neuropathy , anatomy , central nervous system , endocrinology , medicine , biochemistry , diabetes mellitus
Myelin sheath is the proteolipid membrane wrapping the axons of CNS and PNS . We have shown data suggesting that CNS myelin conducts oxidative phosphorylation ( OXPHOS ), challenging its role in limiting the axonal energy expenditure. Here, we focused on PNS myelin. Samples were: (i) isolated myelin vesicles ( IMV ) from sciatic nerves, (ii) mitochondria from primary Schwann cell cultures, and (iii) sciatic nerve sections, from wild type or Charcot‐Marie‐Tooth type 1A ( CMT 1A) rats. The latter used as a model of dys‐demyelination. O 2 consumption and activity of OXPHOS proteins from wild type (Wt) or CMT 1A sciatic nerves showed some differences. In particular, O 2 consumption by IMV from Wt and CMT 1A 1‐month‐old rats was comparable, while it was severely impaired in IMV from adult affected animals. Mitochondria extracted from CMT 1A Schwann cell did not show any dysfunction. Transmission electron microscopy studies demonstrated an increased mitochondrial density in dys‐demyelinated axons, as to compensate for the loss of respiration by myelin. Confocal immunohistochemistry showed the expression of OXPHOS proteins in the myelin sheath, both in Wt and dys‐demyelinated nerves. These revealed an abnormal morphology. Taken together these results support the idea that also PNS myelin conducts OXPHOS to sustain axonal function.