Abstract:
:The Lama2dy mouse, a model of congenital muscular dystrophy (CMD) by merosin deficiency (MCMD), shows muscle degeneration and dysmyelination of peripheral nerves. Although it has been reported that MCMD reduces acetylcholinesterase (AChE) activity of mouse sciatic nerve, no information is available regarding its action on butyrylcholinesterase (BuChE). Amphiphilic BuChE monomers (G(1)(A), 39%), dimers (G(2)(A), 18%), and tetramers (G(4)(A), 33%), along with hydrophilic tetramers (G(4)(H), 10%), were identified in mouse sciatic nerve. It also contained abundant G(4)(A) (75%) and less G(1)(A), G(2)(A), G(4)(H) and A(12) AChE components. In dystrophic nerves, the BuChE activity increased 2-fold but the proportion of the G(4)(A) form dropped from 33% to 10%. AChE activity decreased and the composition of enzyme forms was unaffected. Lectin interaction studies showed that, in contrast to skeletal muscle, the defect of merosin did not greatly alter the glycosylation of nerve cholinesterases. The anomalous synthesis of BuChE forms in dystrophic nerve may be related with peripheral neuropathy of MCMD.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Moral-Naranjo MT,Cabezas-Herrera J,Vidal CJ,Campoy FJdoi
10.1016/s0304-3940(02)00885-6keywords:
subject
Has Abstractpub_date
2002-10-18 00:00:00pages
155-8issue
3eissn
0304-3940issn
1872-7972pii
S0304394002008856journal_volume
331pub_type
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