𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Anti-GM1 antibodies can block neuronal voltage-gated sodium channels

✍ Scribed by Frank Weber; Reinhardt Rüdel; Peter Aulkemeyer; Heinrich Brinkmeier


Publisher
John Wiley and Sons
Year
2000
Tongue
English
Weight
184 KB
Volume
23
Category
Article
ISSN
0148-639X

No coin nor oath required. For personal study only.

✦ Synopsis


Anti-GM1 antibodies, frequently found in the serum of patients with Guillain-Barré syndrome (GBS), have been suggested to interfere with axonal function. We report that IgG anti-GM1 antibodies, raised in rabbits, can reversibly block the voltage-gated Na(+) channels of nerve cells, thus causing a reduction of the excitatory Na(+) current. The block was, however, only substantial when the antibodies were applied together with rabbit complement factors. A solution containing anti-GM1 sera (dilution 1:100) and complement (1:50) reduced the Na(+) current to 0.5 +/- 0.2 times control (mean value +/- SD). Applications of the antibody by itself, complement by itself, or anti-GM2 or anti-GM4 antibodies (1:100) plus complement had little effect. The complexes of anti-GM1 antibodies and complement factors block the ion-conducting pore of the channel directly. In addition, they increase the fraction of channels that are inactivated at the resting potential and alter channel function by changing the membrane surface charge. The described effects may be responsible for conduction slowing and reversible conduction failure in some GBS patients.


📜 SIMILAR VOLUMES


Primary motor neurons fail to up-regulat
✍ Bryan C. Hains; Joel A. Black; Stephen G. Waxman 📂 Article 📅 2002 🏛 John Wiley and Sons 🌐 English ⚖ 322 KB

Epilepsy occurs in a small proportion of patients with spinal cord injury (SCI), but whether it is due to concomitant traumatic head injury or to changes in cortical motor neurons secondary to axotomy within the spinal cord is not known. Na(v)1.3/brain type III sodium channel expression is up-regula