Antagonism of tetrodotoxin‐ and procaine‐induced axonal blockade by adenine nucleotides in the frog sciatic nerve

Article date: February 1984

By: J. A. Ribeiro, A.M. Sebastião in Volume 81, Issue 2, pages 277-282

The effects of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenosine on compound action potentials were investigated in de‐sheathed frog‐sciatic nerve preparations.

ATP and ADP but not adenosine antagonized the inhibitory action of tetrodotoxin (TTX) on nerve conduction. AMP had little or no antagonistic effect on TTX‐induced axonal block. ATP was more effective than ADP. The effects of the nucleotides were related to the degree of the TTX‐induced inhibition and were more evident where the blockade was more intense.

ATP and ADP but not adenosine antagonized the procaine‐induced axonal blockade which, in some experiments, was completely reversed by these nucleotides. ATP and ADP were of similar potency.

The axonal blockade induced by pentobarbitone was not antagonized by ATP, ADP, AMP or adenosine.

The possibility that ATP stimulates a TTX‐sensitive sodium channel is discussed.

The effects of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenosine on compound action potentials were investigated in de‐sheathed frog‐sciatic nerve preparations.

ATP and ADP but not adenosine antagonized the inhibitory action of tetrodotoxin (TTX) on nerve conduction. AMP had little or no antagonistic effect on TTX‐induced axonal block. ATP was more effective than ADP. The effects of the nucleotides were related to the degree of the TTX‐induced inhibition and were more evident where the blockade was more intense.

ATP and ADP but not adenosine antagonized the procaine‐induced axonal blockade which, in some experiments, was completely reversed by these nucleotides. ATP and ADP were of similar potency.

The axonal blockade induced by pentobarbitone was not antagonized by ATP, ADP, AMP or adenosine.

The possibility that ATP stimulates a TTX‐sensitive sodium channel is discussed.

DOI: 10.1111/j.1476-5381.1984.tb10075.x

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