Abstract
POST-TETANIC potentiation of synaptic potentials is usually attributed to a post-tetanic hyperpolarization of nerve terminals which causes the presynaptic action potentials to be larger in amplitude and more effective in transmission1. Primary potentiation can be detected after even one impulse and has been attributed to a mobilization of transmitter so that more is available for release2. It would be predicted, therefore, that abolition of post-tetanic hyperpolarization should concomitantly abolish post-tetanic potentiation but leave primary potentiation untouched. In the present investigation drugs known to abolish post-tetanic hyperpolarization in peripheral nerve fibres3 have been added to the fluid bathing rat-diaphragm phrenic nerve preparations in vitro.
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