Axotomy-induced alterations in the electrophysiological characteristics of neurons

Titmus, Margaret; Faber, Donald S.

doi:10.1016/0301-0082(90)90039-j

Cited by 262 publications

(167 citation statements)

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“…This report is the first to describe long-lasting hyperexcitability produced in intact axons by localized depolarization. Previous reports focused on decreases rather than increases in excitability, produced by either high-frequency activation of an axon (Debanne, 2004) or axon injury (Titmus and Faber, 1990). Although enhancement of action potential conduction (or reflection) at branch points or in neuronal processes prone to conduction failure has been described, reported examples of enhancement barely outlast the duration of axonal firing or neuromodulatory input responsible for the enhancement (Mar and Drapeau, 1996;Baccus et al, 2000;Evans et al, 2003).…”

Section: Depolarization-induced Lth Of Intact Axon Segmentsmentioning

confidence: 99%

“…Although enhancement of action potential conduction (or reflection) at branch points or in neuronal processes prone to conduction failure has been described, reported examples of enhancement barely outlast the duration of axonal firing or neuromodulatory input responsible for the enhancement (Mar and Drapeau, 1996;Baccus et al, 2000;Evans et al, 2003). A long-term, localized decrease in spike threshold triggered by depolarization during axon injury should counteract the increased probability of conduction failure that occurs in an injured region, e.g., by impedance mismatch when spikes invade normal segments after propagating through axon segments narrowed by injury (Titmus and Faber, 1990) or through thin regenerating neurites (Steffensen et al, 1995). The observation of depolarization-induced LTH in intact axons shows that axonal LTH can be produced by mechanisms other than damming of Na ϩ channels at the proximal stump of a severed axon (Devor and Govrin-Lippmann, 1983;Devor et al, 1993).…”

Section: Depolarization-induced Lth Of Intact Axon Segmentsmentioning

confidence: 99%

See 1 more Smart Citation

Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Weragoda¹,

Ferrer²,

Walters³

2004

J. Neurosci.

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Adaptive, long-term alterations of excitability have been reported in dendrites and presynaptic terminals but not along axons. Persistent enhancement of axonal excitability has been described in proximal nerve stumps at sites of nerve section in mammals, but this hyperexcitability is considered a pathological derangement important only as a cause of neuropathic pain. Identified neurons in Aplysia were used to test the hypothesis that either axonal injury or the focal depolarization that accompanies axonal injury can trigger a local decrease in action potential threshold [long-term hyperexcitability (LTH)] having memory-like properties. Nociceptive tail sensory neurons and a giant secretomotor neuron, R2, exhibited localized axonal LTH lasting 24 hr after a crush of the nerve or connective that severed the tested axons. Axons of tail sensory neurons and tail motor neurons, but not R2, displayed similar localized LTH after peripheral depolarization produced by 2 min exposure to elevated extracellular [K ϩ ]. Neither the induction nor expression of either form of LTH was blocked by saline containing 1% normal [Ca 2ϩ ] during treatment or testing. However, both were prevented by local application of the protein synthesis inhibitors anisomycin or rapamycin. The features of (1) long-lasting alteration by localized depolarization, (2) restriction of alterations to intensely depolarized regions, and (3) dependence of the alterations on local, rapamycin-sensitive protein synthesis are shared with synaptic mechanisms considered important for memory formation. This commonality suggests that relatively simple, accessible axons may offer an opportunity to define fundamental plasticity mechanisms that were important in the evolution of memory.

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Section: Depolarization-induced Lth Of Intact Axon Segmentsmentioning

confidence: 99%

Section: Depolarization-induced Lth Of Intact Axon Segmentsmentioning

confidence: 99%

Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Weragoda¹,

Ferrer²,

Walters³

2004

J. Neurosci.

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“…Another possibility is that activity of the cells may downregulate NF protein even further than normal in a manner analogous to the response of axotomized nerves to a second lesion, which has been shown to result in a significant further decline in NF expression (Tetzlaff, 1989). It is important to recognize that the chronic stimulation ofthe peripheral nerves is likely to activate the cell body retrogradely rather than by reflex activation because of the comparatively small contribution of monosynaptic inputs to synaptic activation of the flexor motoneurons and because the synaptic efficacy is reduced by synaptic dysjunction after axotomy (Mendell et al, 1976;reviewed by Gordon, 1983;Titmus and Faber, 1990). As a result, the effects of chronic stimulation are likely to reflect the abnormally high numbers of action potentials that are conducted in the axotomized nerves, which, under natural conditions, are relatively quiescent (Gordon et al, 1980).…”

Section: Stimulation and Atrophymentioning

confidence: 99%

“…Alterations in physiological parameters include reduced action potential amplitude, decreased after-hyperpolarization duration, and slowed nerve conduction velocity (Kuno et al, 1974;Purves, 1975;Davis et al, 1978;Gustafsson and Pinter, 1984;Foehring et al, 1986;Gordon et al, 1987; for reviews, see Gordon, 1983;Titmus and Faber, 1990). Morphological changes in the cell body, the chromatolytic changes, include decentralization of the nucleolus and dissolution of Nissl substance (Nissl, 1892;Liebermann, 197 1).…”

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confidence: 99%

Axotomy-induced changes in rabbit hindlimb nerves and the effects of chronic electrical stimulation

et al. 1991

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Chronic electrical stimulation and extracellular recording combined with morphological examination of nerves in this study provided a detailed description of the time course and extent of fiber atrophy when the trophic influence of the target was removed by ligation of axotomized nerves and neural activity was replaced by chronic stimulation. The major findings are that decline in amplitude of compound action potentials (CAPs) and fiber diameters is rapid after axotomy and is not reversed or prevented by chronic electrical stimulation, as would be predicted if neural activity played an essential role in maintaining normal fiber caliber. Chronic stimulation had a small short-term sparing effect in the first month after axotomy but was counterproductive over long periods. Comparison of the time course of the decline in CAP amplitude and reduction of fiber diameters with described alterations in mRNA expression of neurofilament protein indicates that the early atrophy is too rapid to be accounted for by reduced synthesis and transport of neurofilaments. It is more likely to result from modification of axonal proteins after axotomy. Replacement of neural activity with stimulation may reduce the initial atrophy but, over longer periods, exacerbates the atrophy, possibly by affecting the synthesis and transport of cytoskeletal proteins. These studies show that the trophic control of nerve fiber size is mediated primarily by functional contacts with peripheral targets and that neural activity plays a relatively small role. Without functional contacts, nerve fibers decline in diameter to stable but lower values. The atrophy was exacerbated by imposing neural activity on the relatively quiescent axotomized neurons.

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“…Axotomy provokes several changes in the electrical properties of adult neurons indicating their potential for functional plasticity (see review by Titmus & Faber, 1990). In axotomized rat sympathetic ganglion cells, one or several spikes trigger an after-depolarization (ADP), instead of the after-hyperpolarization (AHP) invariably observed in control cells (Salnchez-Vives & Gallego, 1993a).…”

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confidence: 99%

Calcium‐dependent chloride current induced by axotomy in rat sympathetic neurons.

Sánchez-Vives

Gallego

1994

The Journal of Physiology

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1. Seven to ten days after sectioning their axons, rat sympathetic neurons were studied using intracellular recording techniques in an in vitro preparation of the superior cervical ganglion. 2. In 75 % of axotomized cells, an after-depolarization (ADP) was observed following spike firing or depolarization with intracellular current pulses. Discontinuous single-electrode voltage-clamp techniques were employed to study the ADP. When the membrane potential was clamped at the resting level just after an action potential, a slow inward current wa.s recorded in cells that showed an ADP. 3. In the presence of ITX and TEA, inward peaks and outward currents were recorded during depolarizing voltage jumps, followed by slowly decaying inward tail currents accompanied by large increases in membrane conductance. The inward peak and tail currents activated between -10 and -20 mV and reached maximum amplitudes around 0 mV. With depolarizing jumps to between +40 and +50 mV, net outward currents were recorded during the depolarizing jumps but inward tail currents were still activated. 4. In the presence of the Ca2+ channel blocker cadmium, or when Ca2+ was substituted by Mg2+, the ADP disappeared. In voltage-clamped cells, cadmium blocked the inward tail currents. The reversal potential for the inward tail current was approximately -15 mV.

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Axotomy-induced alterations in the electrophysiological characteristics of neurons

Cited by 262 publications

References 332 publications

Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Axotomy-induced changes in rabbit hindlimb nerves and the effects of chronic electrical stimulation

Calcium‐dependent chloride current induced by axotomy in rat sympathetic neurons.

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