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Serge Lafontaine^*, Michael Rasminsky^*,, Takahiko Saida and Austin J. Sumner

Neurosciences Unit, Montreal General Hospital, Department of Neurology and Neurosurgery, McGill University, 1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada

Department of Neurology, University of Pennsylvania, Philadelphia, PA 19104, U.S.A.

1. We have observed conduction in single rat spinal ventral root nerve fibres following acute topical application of anti-galactocerebroside serum.

2. Conduction of nerve impulses was initially slowed and subsequently blocked at the site of serum exposure.

3. Conduction block occurred within as little as 1 hr in more slowly conducting (20-30 m/sec) myelinated fibres but occurred later in fibres conducting more rapidly.

4. Conduction block was preceded by a rise in internodal conduction time from the normal 20 µsec to about 200 µsec.

5. At nodes exposed to serum, conduction block was invariably associated with greatly decreased depolarization; this was contrasted with nodes exposed to local anaesthetic or tetrodotoxin where conduction block occurred despite nodal depolarization well beyond threshold potential.

6. Nodal capacitance and resistance were estimated from simultaneous recordings of membrane current and extracellular potential at blocked nodes exposed to local anaesthetic or tetrodotoxin (normal nodes) and at blocked nodes exposed to anti-galactocerebroside serum.

7. For normal fibres of internodal length 0·8-1·1 mm, an upper limit estimate for average nodal capacitance was 2·6 ± 0·3 pF and a lower limit estimate for average nodal resistance was 55 ± 10 M. There was an order of magnitude increase in the capacitance of nodes at which conduction block occurred following exposure to anti-galactocerebroside serum.

8. We conclude that the early conduction block caused by anti-galactocerebroside serum is due to paranodal demyelination and that acute paranodal demyelination is sufficient to cause conduction block.

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