Post-tetanic depolarization in sympathetic neurones of the guinea-pig.

1. Repetitive intracellular stimulation at a frequency of 5-30 Hz for 1-10 s evoked in neurones of the isolated inferior mesenteric and superior cervical ganglia of the guinea-pig three types of post-spike membrane potential changes: (i) hyperpolarization, (ii) hyperpolarization followed by a slow depolarization, and (iii) a second hyperpolarization following the initial two responses.2. The initial post-spike hyperpolarization had a mean duration of 2.0 s and was often associated with a fall in membrane resistance; it could be elicited in every sympathetic neurone studied. This response was termed the post-tetanic hyperpolarization (PTH).3. The slow depolarization which could be induced only in a portion of neurones had a mean amplitude and duration of 2.2 mV and 27.5 s, respectively; it was termed the post-tetanic depolarization (PTD).4. PTD was associated with a fall in membrane resistance, augmented by membrane hyperpolarization, and reduced by depolarization; its mean extrapolated equilibrium potential was -38 mV.5. PTD was not blocked by nicotinic and muscarinic antagonists, or alpha-and beta-adrenergic receptor antagonists, whereas it was suppressed by adrenaline, noradrenaline, Co(2+) and a low Ca(2+) solution.6. The amplitude of the single spike after-hyperpolarization in normal Krebs solution as well as in high K(+) solution was increased during PTD; furthermore, conditioning hyperpolarization to the level of E(K) increased the amplitude of PTD in normal Krebs as well as in high K(+) solution.7. PTD with similar amplitude, time course and membrane characteristics could be evoked in a portion of neurones of the rabbit superior cervical ganglia; however, PTD was not detected in neurones of the rat superior cervical ganglia.8. Decentralization of the guinea-pig and rabbit superior cervical ganglia for 14 d did not alter the number of neurones in which PTD could be elicited, its amplitude, or its time course.9. Our results suggest that a chemical substance(s) is responsible for the generation of PTD; it may be released from the soma and/or dendrites and acts in an auto-receptive manner on the cells in question. The nature and origin of the second hyperpolarization remain to be clarified.