Potassium depletion and the central action of curare.

PELOUZE and Bernard (1850) first described the peripheral nature of curare paralysis. Further investigation, begun in 1852 by Claude Bernard, demonstrated the action of curarine to be at the neuromuscular junction (Bernard, 1856). Thus, one hundred years ago, the idea crystallized that the central actions of curare were unimportant or nonexistent, and was given form by such statements as " Mais c'est le contraire qui a lieu, et le curare n'a que l'apparence d'etre un agent anesthetique, car l'animal sent, mais il ne peut pas le manifester" (Bernard, 1857); and " La sensibilite est conserve dans l'empoisonnement par le curare; mais cette sensibilite est muette, elle a perdu tous ses moyens d'expression qui sont les nerfs moteur " (Vulpian, 1856). In this way was curare relegated to a class of drugs having only a peripheral action in the animal body, and even today is so classified, despite abundant pharmacological evidence of its central effect in experimental preparations, notably described by Salama and Wright (1950, 1952b), whose work was in a tradition dating back to Tillie (1890), of Edinburgh, the first to suggest a similarity between strychnine and curare.