Posttetanic changes in membrane potential of single medullated nerve fibers

Gm, Schoepfle; Cr, Katholi

doi:10.1152/ajplegacy.1973.225.6.1501

Cited by 23 publications

(16 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This conclusion was later confirmed by Schoepfle & Katholi (1973), who also used Li+ solutions to block the membrane hyperpolarization. However, this view has been challenged recently by Bergman, Dubois & Bergman (1980) who claimed that the post-tetanic hyperpolarization, though related to the sodium pump, is not due to the pump being electrogenic but due to extracellular potassium depletion.…”

Section: H Bostock and P Grafementioning

confidence: 70%

Activity‐dependent excitability changes in normal and demyelinated rat spinal root axons.

Bostock¹,

Grafe²

1985

The Journal of Physiology

258

199

View full text Add to dashboard Cite

SUMMARY1. Myelinated nerve fibres with a reduced safety factor for conduction due to demyelination are easily blocked by trains of impulses. To find out why, in vivo recordings from rat ventral root fibres demyelinated with diphtheria toxin have been supplemented with in vivo and in vitro recordings from normal fibres.2. Despite a small rise in extracellular potassium activity, normal fibres were invariably hyperpolarized by intermittent trains of impulses. This hyperpolarization resulted in an increase in threshold and also in an enhancement of the depolarizing after-potential and the superexcitable period.3. Replacement of NaCl in the extracellular solution by LiCl completely blocked both the membrane hyperpolarization and the threshold increase which were normally observed during intermittent trains of impulses. 4. At demyelinated nodes which were blocked by trains of impulses (10-50 Hz), conduction block was preceded by a rise in threshold current and an increase in internodal conduction time, but by no detectable reduction in the outward current generated by the preceding node. 5. It was found possible to prevent the threshold from changing during a train by automatic adjustment of a d.c. polarizing current. This 'threshold clamp' prevented the conduction failure and virtually abolished the changes in internodal conduction time.6. The threshold changes were attributed to hyperpolarization, as in normal fibres, since (a) the polarizing current required to prevent them was always a depolarizing current, and (b) they were accompanied by an increase in superexcitability.7. The post-tetanic depression that can follow continuous trains of impulses was attributed to the combination of increased threshold and enhanced superexcitable period due to hyperpolarization.8. It is concluded that the susceptibility of these demyelinated fibres to impulse trains is not due to a membrane depolarization induced by extracellular potassium accumulation but to a membrane hyperpolarization as a consequence of electrogenic sodium pumping.

show abstract

Section: H Bostock and P Grafementioning

confidence: 70%

Activity‐dependent excitability changes in normal and demyelinated rat spinal root axons.

Bostock¹,

Grafe²

1985

The Journal of Physiology

258

199

View full text Add to dashboard Cite

show abstract

“…Long trains of impulses induce hyperpolarization of peripheral axons due to activation of the Na + –K + pump by Na + entry (Ritchie & Straub, 1957; Bergmans & Michaux, 1970; Schoepfle & Katholi, 1973; Bostock & Grafe, 1985).…”

Section: Resultsmentioning

confidence: 99%

Mechanisms of hyperpolarization in regenerated mature motor axons in cat

Moldovan

Krarup

2004

The Journal of Physiology

View full text Add to dashboard Cite

We found persistent abnormalities in the recovery of membrane excitability in long-term regenerated motor nerve fibres in the cat as indicated in the companion paper. These abnormalities could partly be explained by membrane hyperpolarization. To further investigate this possibility, we compared the changes in excitability in control nerves and long-term regenerated cat nerves (3-5 years after tibial nerve crush) during manoeuvres known to alter axonal membrane Na + -K + pump function: polarization, cooling to 20• C, reperfusion after 10 min ischaemia, and up to 60 s of repetitive stimulation at 200 Hz. The abnormalities in excitability of regenerated nerves were reduced by depolarization and cooling and increased by hyperpolarization and during postischaemia. Moreover, the time course of recovery of excitability from repetitive stimulation and ischaemia was prolonged in regenerated nerves. Our data are consistent with an increased demand for electrogenic Na + -K + pumping in regenerated nerves leading to membrane hyperpolarization. Such persistent hyperpolarization may influence the ability of the axon to compensate for changes in membrane potential following normal repetitive activity.

show abstract

“…3,7,24 The mechanisms responsible for hyperpolarization are believed to be dependent on the length of the impulse train: activation of nodal slow K conductance following brief trains, 3,24 and activation of the electrogenic Na + /K + pump with longer trains. 4,6,19,20 Although both phenomena are thought to occur in human motor and sensory axons, 2,17,18,[22][23][24] it is not clear whether rate-dependent excitability change has a role in the symptomatology or pathophysiology of human neuropathies.In demyelinating neuropathy, conduction block (after a single impulse) of the sensory fibers is considered to be associated with impairment of elementary sensations such as touch, pin-prick, or position. More complicated sensations, such as vibratory sensation and texture discrimination, may be affected by activity-dependent conduction block or the exact timing of train impulses.…”

mentioning

confidence: 99%