4.5 Article

Acute motor deficit and subsequent remyelination-associated recovery following internal capsule demyelination in mice

期刊

JOURNAL OF NEUROCHEMISTRY
卷 156, 期 6, 页码 917-928

出版社

WILEY
DOI: 10.1111/jnc.15142

关键词

demyelination; internal capsule; lysophosphatidylcholine; motor recovery; remyelination

资金

  1. SENSHIN Medical Research Foundation
  2. Jichi Medical University [30-5]
  3. National Center of Neurology and Psychiatry
  4. Setsuro Fujii Memorial, Osaka Foundation for Promotion of Fundamental Medical Research
  5. National Multiple Sclerosis Society [JF-1806-31381]
  6. Congressionally Directed Medical Research Programs [W81XWH-17-1-0268]
  7. National Institutes of Health [R01NS107523]

向作者/读者索取更多资源

The study found that focal IC demyelination induced by LPC injection resulted in acute motor deficit, but the mice regained motor function and axonal integrity in lesions by 28 days post-lesion through remyelination.
Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system (CNS), characterized by accumulated motor disability. However, whether remyelination promotes motor recovery following demyelinating injury remains unclear. Damage to the internal capsule (IC) is known to result in motor impairment in multiple sclerosis and stroke. Here, we induced focal IC demyelination in mice by lysophosphatidylcholine (LPC) injection, and examined its effect on motor behavior. We also compared the effect of LPC-induced IC damage to that produced by endothelin-1 (ET1), a potent vasoconstrictor used in experimental stroke lesions. We found that LPC or ET1 injections induced asymmetric motor deficit at 7 days post-lesion (dpl), and that both lesion types displayed increased microglia/macrophage density, myelin loss, and axonal dystrophy. The motor deficit and lesion pathology remained in ET1-injected mice at 28 dpl. In contrast, LPC-injected mice regained motor function by 28 dpl, with corresponding reduction in activated microglia/macrophage density, and recovery of myelin staining and axonal integrity in lesions. These results suggest that LPC-induced IC demyelination results in acute motor deficit and subsequent recovery through remyelination, and may be used to complement future drug screens to identify drugs for promoting remyelination.

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