Axonal transport in rats rendered paraplegic following a single subarachnoid injection of either batrachotoxin or 6‐aminonicotinamide into the spinal cord

Abstract

Batrachotoxin (BTX) or 6-aminonicotinamide (6-AN) when injected into the subarachnoidal space of the lumbar spinal cord block fast axonal transport of 3H-protein in motor nerves. Axonal transport recovers partially within one day after administering BTX while the effect of 6-AN lasts for more than 21 days. These observations are discussed in relation to the onset and recovery of membrane depolarization observed in the extensor muscle.

Dependence of batrachotoxin block of axoplasmic transport on sodium

“…We would expect that BTX when injected centrally would act similarly to its effect in peripheral nerve, namely, to block transport in the motoneuron axons exposed to the agent (cf. Warnick and Albuquerque, 1978;Boegman and Albuquerque, 1980).…”

“…A similar high activity of BTX was found by Warnick and Albuquerque (1978) who reported the development of flaccid paralysis associated with electrophysiologic evidence of muscular denervation in rats following the injection of BTX into the lumbar subarachnoid space. They also presented evidence that the effects of such injections were most likely due to a block of axoplasmic transport (Boegman and Albuquerque, 1980). Batrachotoxin has been shown to block electrical activity in nerve and in muscle by increasing resting membrane permeability to Na+ and altering Na+ activation (Narahashi, Albuquerque, and Deguchi, 1971;Khodorov and Revenko, 1979).…”