Action Potentials in Chick Atria: INCREASED SUSCEPTIBILITY TO BLOCKADE BY TETRODOTOXIN DURING EMBRYONIC DEVELOPMENT

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Abstract
Tetrodotoxin (TTX) at a concentration of 1.6 x 10-7M blocked intracellularly recorded action potentials in 12- and 18-day-old embryonic chick atria. However, TTX, 1 x 10-5M, did not abolish action potentials recorded from cells in 6-day-old atria. TTX-sensitive receptor sites were present in 6-day-old atrial membranes because the toxin depressed the early Na+ conductance that generated the rapid depolarization phase and the maximum rate of rise of the action potential. TTX at 0.9 x 10-8M reduced the maximum rate of rise by 50% in 6-day-old atria, and TTX at 2 x 10-8M had the same effect in 12- and 18-day-old preparations. Action potential overshoot changed about 10-20 mv/tenfold variation in external Na+ concentration in 6-day-old atria in contrast to the change of about 60 mv/decade observed in 18-day-old atria. Moreover, the TTX-resistant action potentials in 6-day-old atria depended primarily on an inward Ca2+ current because overshoot changed 24 mv/decade variation in external Ca2+ concentration. The improvement in sodium-electrode properties that occurred during maturation was accompanied by an increase in the maximum rate of rise of the action potential, which averaged 64 v/sec in 6-day-old atria and 94 v/sec in 18-day-old atria. These findings suggested that the early Na+ conductance mechanism became more critical in generating the action potential in older embryonic atria. These data were consistent with the hypothesis that the membrane density of early conductance sites increased with embryonic age. The TTX resistance of 6-day-old atria depended on an inward Ca2+ current that generated action potentials after the early Na+ conductance sites had been blocked by the toxin.