The hyperpolarization which follows activity in mammalian non‐medullated fibres

Ritchie, J. M.; Straub, R. W.

doi:10.1113/jphysiol.1957.sp005744

Cited by 255 publications

(169 citation statements)

References 17 publications

(25 reference statements)

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“…Activity-dependent hyperpolarization of the axon usually results from activation of the Na + /K + ATPase and/or activation of calcium-dependent potassium channels. Unmyelinated axons in the PNS (for example, vagal C-fibres) hyperpolarize in response to repeated action potentials 93,94 as a result of the intracellular accumulation of sodium ions and the subsequent activation of the electrogenic Na + /K + pump 26,93,94 . In crayfish axons, this hyperpolarization can have a magnitude of 5-10 mV (REF.…”

Section: Geometrical Factors: Branch Points and Swellingsmentioning

confidence: 99%

Information processing in the axon

2004

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Section: Geometrical Factors: Branch Points and Swellingsmentioning

confidence: 99%

Information processing in the axon

2004

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“…The phenomenon of post-spike activity has been analysed in a variety of preparations, for example, myelinated (Straub, 1961) and unmyelinated (Ritchie & Straub, 1957) nerve fibres, leech ganglion cells (Baylor & Nicholls, 1969), crayfish stretch receptors (Nakajima & Takahashi, 1966), cat dorsal spinocerebellar tract neurones (Kuno et al 1970), Aplysia giant neurones (Brodwick & Junge, 1972) and bullfrog sympathetic ganglion cells (Koketsu, 1971;Minota, 1974). In all these tissues, post-stimulus membrane activity consisted of a hyperpolarization which was not followed by depolarization.…”

Section: Discussionmentioning

confidence: 99%

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

Dun

Minota

1982

The Journal of Physiology

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SUMMARY1. 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 a-and /1-adrenergic receptor antagonists, whereas it was suppressed by adrenaline, noradrenaline, Co2+ and a low Ca2+ 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 EK 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 substances) 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.

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“…In mammalian non-medullated nerve fibres a short burst of activity is followed by a pronounced post-tetanic hyperpolarization (Brown & Holmes, 1956). This hyperpolarization was shown by Ritchie & Straub (1957) to be quickly decreased by 2:4-dinitrophenol, azide, cyanide and iodoacetate, compounds known to block metabolic pathways, suggesting that the hyperpolarization is dependent on metabolic processes. In the present experiments we investigated whether lack of glucose, the only fuel ordinarily present in Locke's solution, might cause a decrease in the post-tetanic hyperpolarization.…”

Section: P Proceedings Of the Physiologicalmentioning

confidence: 97%

Proceedings of the Physiological Society

1957

The Journal of Physiology

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The hyperpolarization which follows activity in mammalian non‐medullated fibres

Cited by 255 publications

References 17 publications

Information processing in the axon

Information processing in the axon

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

Proceedings of the Physiological Society

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