Evaluation of Na+/K+ pump function following repetitive activity in mouse peripheral nerve

Moldovan, Mihai; Krarup, Christian

doi:10.1016/j.jneumeth.2005.12.015

Cited by 30 publications

(38 citation statements)

References 43 publications

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“…Earlier studies showed that application of subthreshold polarizing currents up to 0.2 s duration as part of the routine TROND protocol in mice did not cause a substantial polarization of these electrodes (Moldovan et al, 2009). Consistent with previous observations, mouse motor axons accommodated in seconds to hyperpolarization (Boërio et al, 2009; Moldovan and Krarup, 2006). Furthermore, here we found that maintaining hyperpolarization for minutes did not cause an additional substantial sag in the threshold current (Fig.…”

Section: Methodssupporting

confidence: 92%

In vitro electrophoresis and in vivo electrophysiology of peripheral nerve using DC field stimulation

Madison

Robinson

Krarup

et al. 2014

Journal of Neuroscience Methods

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Background Given the movement of molecules within tissue that occurrs naturally by endogenous electric fields, we examined the possibility of using a low-voltage DC field to move charged substances in rodent peripheral nerve in vitro. New Method Labeled sugar- and protein-based markers were applied to a rodent peroneal nerve and then a 5–10 V/cm field was used to move the molecules within the extra- and intraneural compartments. Physiological and anatomical nerve properties were also assessed using the same stimulation in vivo. Results We demonstrate in vitro that charged and labeled compounds are capable of moving in a DC field along a nerve, and that the same field applied in vivo changes the excitability of the nerve, but without damage. Conclusions The results suggest that low-voltage electrophoresis could be used to move charged molecules, perhaps therapeutically, safely along peripheral nerves.

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Section: Methodssupporting

confidence: 92%

In vitro electrophoresis and in vivo electrophysiology of peripheral nerve using DC field stimulation

Madison

Robinson

Krarup

et al. 2014

Journal of Neuroscience Methods

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“…We show that the STS effect is due to the Na + /K + pump (Figure 3). It has been proposed for many axons that slow hyperpolarization and slowing of conduction is caused by this pump, which is activated by the massive Na + influx during repetitive spiking and causes a net deficit of positive charge (Van Essen, 1973; Gordon et al, 1990; Bostock and Bergmans, 1994; Robert and Jirounek, 1994; Vagg et al, 1998; Baker, 2000; Kiernan et al, 2004; Moldovan and Krarup, 2006; Scuri et al, 2007). Direct experimental evidence of the involvement of the pump in activity-dependent dynamics for the PD axon is missing because of the difficulty that pharmacological block of the pump also interferes with its overall role in maintaining a functional membrane potential (Ballo and Bucher, 2009).…”

Section: Discussionmentioning

confidence: 99%

Ionic mechanisms underlying history-dependence of conduction delay in an unmyelinated axon

Zhang

Bucher

Nadim

2017

eLife

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Axonal conduction velocity can change substantially during ongoing activity, thus modifying spike interval structures and, potentially, temporal coding. We used a biophysical model to unmask mechanisms underlying the history-dependence of conduction. The model replicates activity in the unmyelinated axon of the crustacean stomatogastric pyloric dilator neuron. At the timescale of a single burst, conduction delay has a non-monotonic relationship with instantaneous frequency, which depends on the gating rates of the fast voltage-gated Na+ current. At the slower timescale of minutes, the mean value and variability of conduction delay increase. These effects are because of hyperpolarization of the baseline membrane potential by the Na+/K+ pump, balanced by an h-current, both of which affect the gating of the Na+ current. We explore the mechanisms of history-dependence of conduction delay in axons and develop an empirical equation that accurately predicts this history-dependence, both in the model and in experimental measurements.DOI: http://dx.doi.org/10.7554/eLife.25382.001

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“…The repolarization undershoots and causes hyperpolarization [19]. The hyperpolarization is due to the action of the sodium-dependent Na + /K + -pump that exchanges three intracellular Na + ions for two extracellular K + ions, resulting in a net outwards current [27–29]. …”

Section: Discussionmentioning

confidence: 99%

“…Although the inhibition mechanism of the Na + /K + -pump could also be activated during HFS since ion concentrations were changing in the intracellular and extracellular spaces. But the effect might be too weak and slow to overcome the strong and rapid depolarization effects of stimulation pulses [22, 27]. Therefore, only after the cease of HFS would the hyperpolarization effects of Na + /K + -pump dominate the membrane potentials of axons and form the slow recovery of stage 2.…”

Section: Discussionmentioning

confidence: 99%

High Frequency Stimulation Extends the Refractory Period and Generates Axonal Block in the Rat Hippocampus

Feng

Guo

et al. 2014

Brain Stimulation

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Background The therapeutic mechanisms of deep brain stimulations (DBS) are not fully understood. Axonal block induced by high frequency stimulation (HFS) has been suggested as one possible underlying mechanism of DBS. Objective To investigate the mechanism of the generation of HFS-induced axonal block. Methods High frequency pulse trains were applied to the fiber tracts of alveus and Schaffer collaterals in the hippocampal CA1 neurons in anaesthetized rats at 50, 100 and 200 Hz. The amplitude changes of antidromic-evoked population spikes (APS) were measured to determine the degree of axonal block. The amplitude ratio of paired-pulse evoked APS was used to assess the changes of refractory period. Results There were two distinct recovery stages of axonal block following the termination of HFS. One frequency-dependent faster phase followed by another frequency-independent slower phase. Experiments with specially designed temporal patterns of stimulation showed that HFS produced an extension of the duration of axonal refractory period thereby causing a fast recovery phase of the axonal block. Thus, prolonged gaps inserted within HFS trains could eliminate the axonal block and induced large population spikes and even epileptiform activity in the upstream or downstream regions. Conclusions Extension of refractory period plays an important role on HFS induced axonal block. Stimulation pattern with properly designed pauses could be beneficial for different requirements of excitation or inhibition in DBS therapies.

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Evaluation of Na+/K+ pump function following repetitive activity in mouse peripheral nerve

Cited by 30 publications

References 43 publications

In vitro electrophoresis and in vivo electrophysiology of peripheral nerve using DC field stimulation

In vitro electrophoresis and in vivo electrophysiology of peripheral nerve using DC field stimulation

Ionic mechanisms underlying history-dependence of conduction delay in an unmyelinated axon

High Frequency Stimulation Extends the Refractory Period and Generates Axonal Block in the Rat Hippocampus

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