Ionic and metabolic dependence of axotomy‐induced somatic membrane changes in crayfish.

Kuwada, John Y.

doi:10.1113/jphysiol.1981.sp013836

Cited by 16 publications

(11 citation statements)

References 21 publications

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“…Evidence in the following paper indicates that excitability is actually reversed and not merely masked (Kuwada, 1981). The reversal might occur either because the signal that initiated the changes is itself reversed or because the changes are self-limiting.…”

Section: Discussionmentioning

confidence: 83%

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Transient, axotomy‐induced changes in the membrane properties of crayfish central neurones.

Kuwada¹,

Wine²

1981

The Journal of Physiology

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SUMMARY1. In crayfish, the normally passive, non-spiking somata of certain unipolar, efferent neurones became spiking within 36 hr of axotomy.2. The changes persisted for approximately 2 weeks and then waned. The decline in excitability occurred independently of regeneration, and excitability was not restored by recutting 'the axon stump.3. The neuropilar processes also became capable of supporting spikes, but synaptic transmission onto the cells and the spike threshold for orthodromic activation were unchanged, as was the gross structure of the neurone.4. In somata which normally spike, electrogenicity was nevertheless increased, as evidenced by soma spikes that were larger, faster rising, and easier to evoke.5. We tested for post-axotomy excitability changes in a variety of identified neurones. Every type (n = 5) of phasically active efferent we tested responded as above, as did all three phasic interneurones. One class of spontaneously active interneurones and one spontaneously active efferent did not respond to axotomy.6. Extensive damage to afferents did not initiate changes in efferents of the same ganglion, nor did it interfere with changes induced by axotomy of the efferents.7. Transection of the larger of the two main branches of the phasic flexor inhibitor induced soma excitability, but cutting the smaller branch did not. However, after the excitability caused by cutting the larger branch waned, transaction of the smaller branch then induced excitability.8. Neurones with longer axon stumps took longer to develop soma excitability.

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Section: Discussionmentioning

confidence: 83%

“…However, high rates of activity presumably pose a greater metabolic burden on neurones and that may be relevant to their response to axotomy. In this regard, evidence is presented in the following paper that the axotomy-induced changes depend upon protein synthesis (Kuwada, 1981).…”

Section: Discussionmentioning

confidence: 99%

Transient, axotomy‐induced changes in the membrane properties of crayfish central neurones.

Kuwada¹,

Wine²

1981

The Journal of Physiology

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“…This view, although possible, fails to take into account the evidence for greatly increased protein synthesis following axotomy (1,23) as well as the evidence in invertebrates that protein synthesis is critical for the appearance of axotomy-induced Na' spikes in proximal regions of the neuron where they were formerly absent (19). We therefore prefer explanations that involve Na'-channel protein synthesis.…”

Section: Resultsmentioning

confidence: 97%

“…A reasonable explanation for the source of the Na' currents is that they reflect manufacture of new Na' channels at the normal or even at an increased rate in response to axotomy (19). These channels are intended for the regenerating axon but are concentrated in all regions above the lesion, particularly near the soma, and are inserted in the somadendritic membranes.…”

Section: Resultsmentioning

confidence: 99%

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Sernagor¹,

Yarom²,

Werman³

1986

Proc. Natl. Acad. Sci. U.S.A.

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Ten days after extradural axotomy, partial spikes are found in >20% of cat L7 motoneurons, while 15-21 days after axotomy the incidence increases to 60%. These responses are produced in excitable (hot) spots in the dendrites by synaptic excitation. Intracellular injection of a lidocaine derivative and effective blocker of Na+ channels from within neurons, results in elimination of partial spikes before blocking somadendritic spikes. Partial spikes appear rather abruptly '.10 days after axotomy in our hands, are present in 23.6% of 106 neurons 10-14 days after axotomy, and the incidence more than doubles to 60.0% of 90 neurons 15-21 days after axotomy. Initially, a number of experiments were carried out in Abbreviations: EPSP, excitatory postsynaptic potential; PBST, posterior biceps-semitendinosus; LGS, lateral gastrocnemiussoleus; MG, medial gastrocnemius. 7966The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…Such axotomy-induced soma excitability has also been shown in some vertebrate neurons (for review, Titmus and Faber, 1990). The ionic basis of axotomyinduced soma excitability has been examined directly, using pharmacological manipulations of ionic conductances in these vertebrate (Titmus and Faber, 1990) and invertebrate neurons (Goodman and Heitler, 1979;Pitman, 1979;Kuwada, 1981). In all cases, the enhanced excitability appeared to depend on voltage-dependent Na + conductances.…”

Section: Introductionmentioning

confidence: 98%

Ionic Dependence of the Axotomy-Induced Long-Lasting Firing in an Identified Crayfish Motoneuron

Muramoto¹

1998

Zoological Science

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I have reported previously that axotomy of an identifiable anal motoneuron of crayfish Procambarus clarkii induces a long-lasting firing and that a prolonged depolarizing pulse to its cut end can induce a similar response. In this study, I confirmed that this stimulus is comparable to axotomy; the frequency of stimulus-induced firing increases linearly with the stimulus intensity and its firing pattern is the same as that following axotomy. Then, when the cut end was bathed for more than 1 hr in test solutions, it was examined whether the stimulus to the cut end induces or blocks the response. Na(+)-free saline (Tris(+) replaced Na(+)) or TTX (3 x 10(-7) M) reversibly blocked the response within 30 min. By contrast, Mn(2+) saline (40 mM Mn(2+) replaced Ca(2+)) or Ca(2+)-free salines (Mg(2+) or 1 mM EDTA replaced Ca(2+)) cannot block the response, but instead increased the firing frequency. These results obtained with stimulus were confirmed also by those with axotomy. I concluded that axotomy-induced firing, which occurs locally at its cut region, is primarily responsible for voltage-dependent Na(+) conductances, but not for Ca(2+) ones.

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Ionic and metabolic dependence of axotomy‐induced somatic membrane changes in crayfish.

Cited by 16 publications

References 21 publications

Transient, axotomy‐induced changes in the membrane properties of crayfish central neurones.

Transient, axotomy‐induced changes in the membrane properties of crayfish central neurones.

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Ionic Dependence of the Axotomy-Induced Long-Lasting Firing in an Identified Crayfish Motoneuron

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