Post‐tetanic depolarization in sympathetic neurones of the guinea‐pig

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Abstract
Repetitive intracellular stimulation at a frequency of 5-30 Hz for 1-10 s evoked, in neurons of the isolated inferior mesenteric and superior cervical ganglia of the guinea pig, 3 types of post-spike membrane potential changes: hyperpolarization, hyperpolarization followed by a slow depolarization, and a 2nd hyperpolarization following the initial 2 responses. 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 neurons studied. This response was termed the post-tetanic hyperpolarization (PTH). The slow depolarization which could be induced only in a portion of neurons had a mean amplitude and duration of 2.2 mV and 27.5 s, respectively; it was termed the post-tetanic depolarization (PTD). 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. PTD was not blocked by nicotinic and muscarinic antagonists, or .alpha.- and .beta.-adrenergic receptor antagonists, whereas it was suppressed by adrenaline [epinephrine] noradrenaline [norepinephrine] CO2+ and a low Ca2+ solution. 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 EK [equilibrium potential for K+] increased the amplitude of PTD in normal Krebs as well as in high K+ solution. PTD with similar amplitude, time course and membrane characteristics could be evoked in a portion of neurons of the rabbit superior cervical ganglia; however, PTD was not detected in neurons of the rat superior cervical ganglia. Decentralization of the guinea pig and rabbit superior cervical ganglia for 14 days did not alter the number of neurons in which PTD could be elicited, its amplitude, or its time course. 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 2nd hyperpolarization remain to be clarified.