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Post‐tetanic depolarization in sympathetic neurones of the guinea‐pig
Author(s) -
Dun N. J.,
Minota S.
Publication year - 1982
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1982.sp014075
Subject(s) - hyperpolarization (physics) , depolarization , membrane potential , chemistry , tetanic stimulation , biophysics , spike potential , stimulation , excitatory postsynaptic potential , medicine , biology , biochemistry , receptor , stereochemistry , nuclear magnetic resonance spectroscopy
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 α‐and β‐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.