Retrograde transport of plasticity signals in Aplysia sensory neurons following axonal injury

Gunstream, JD; Castro, Gilbert A.; Walters, E. T.

doi:10.1523/jneurosci.15-01-00439.1995

Cited by 62 publications

(74 citation statements)

References 40 publications

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“…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). The distance of the treated nerve segment from the neuronal soma (2-4 cm) and the blockade of synaptic transmission in the ganglion during induction and testing of LTH, coupled with reported rates of axonal transport in Aplysia (ϳ1.5 mm/hr) (Ambron et al, 1992;Gunstream et al, 1995;Sung et al, 2004), suggests that the axonal LTH seen 24 hr after treatment does not depend on transport of retrograde signals that produce transcriptional or translational effects in the soma Sung et al, 2004) and subsequent anterograde transport of plasticity-mediating molecules to the axonal test site.…”

Section: Depolarization-induced Lth Of Intact Axon Segmentsmentioning

confidence: 95%

“…Nerve p9 or the RPAC was crushed using fine forceps 0.5-4 mm distal to the test slot in the configuration shown in Figure 1 A or in the middle of the test well in the configuration shown in Figure 1 B (Gunstream et al, 1995). The distance from the end of the slot to the crush site was measured after the 24 hr test.…”

Section: Methodsmentioning

confidence: 99%

“…We next examined axons of identified tail motor neurons, which, like tail sensory neurons, project their axons into peripheral nerve p9 (Walters et al, 1983) and display LTH in the cell body after axotomy Gunstream et al, 1995;Ambron et al, 1996). Moreover, several studies indicate that motor neurons in Aplysia may be sites of short-and long-term memory storage (Trudeau and Castellucci, 1995;Zhu et al, 1997;Roberts and Glanzman, 2003).…”

Section: Tail Motor Neuron Axons Display Lth After High-k Treatmentmentioning

confidence: 99%

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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: 95%

Section: Methodsmentioning

confidence: 99%

Section: Tail Motor Neuron Axons Display Lth After High-k Treatmentmentioning

confidence: 99%

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Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Weragoda¹,

Ferrer²,

Walters³

2004

J. Neurosci.

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“…This nanorod-containing cargo diffused freely in the axon of a differentiated PC12 cell, which had been treated with colchicine to destroy the microtubules ( Supplementary Fig. S3) 43 . As the cargo could no longer attach to the intact microtubules, it performed random translational and rotational diffusion.…”

Section: Rotation Of Endocytic Vesicles Reported By Gold Nanorodsmentioning

confidence: 99%

Rotational dynamics of cargos at pauses during axonal transport

Sun

Wang

et al. 2012

Nat Commun

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Direct visualization of axonal transport in live neurons is essential for our understanding of the neuronal functions and the working mechanisms of microtubule-based motor proteins. Here we use the high-speed single particle orientation and rotational tracking technique to directly visualize the rotational dynamics of cargos in both active directional transport and pausing stages of axonal transport, with a temporal resolution of 2 ms. Both long and short pauses are imaged, and the correlations between the pause duration, the rotational behaviour of the cargo at the pause, and the moving direction after the pause are established. Furthermore, the rotational dynamics leading to switching tracks are visualized in detail. These first-time observations of cargo's rotational dynamics provide new insights on how kinesin and dynein motors take the cargo through the alternating stages of active directional transport and pause.

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“…Two studies support this idea. First, blocking axonal transport after nerve injury in excised nervous systems prevented the appearance of LTH (Gunstream et al, 1995). Second, LTH was induced in noninjured SNs by injecting axoplasm from injured axons (Ambron et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

A Neuronal Isoform of Protein Kinase G Couples Mitogen-Activated Protein Kinase Nuclear Import to Axotomy-Induced Long-Term Hyperexcitability inAplysiaSensory Neurons

Sung¹,

Walters²,

Ambron³

2004

J. Neurosci.

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The induction of a long-term hyperexcitability (LTH) in vertebrate nociceptive sensory neurons (SNs) after nerve injury is an important contributor to neuropathic pain in humans, but the signaling cascades that induce this LTH have not been identified. In particular, it is not known how injuring an axon far from the cell soma elicits changes in gene expression in the nucleus that underlie LTH. The nociceptive SNs of Aplysia (ap) develop an LTH with electrophysiological properties after axotomy similar to those of mammalian neurons and are an experimentally useful model to examine these issues. We cloned an Aplysia PKG (cGMP-dependent protein kinase; protein kinase G) that is homologous to vertebrate type-I PKGs and found that apPKG is activated at the site of injury in the axon after peripheral nerve crush. The active apPKG is subsequently retrogradely transported to the somata of the SNs, but apPKG activity does not appear in other neurons whose axons are injured. In the soma, apPKG phosphorylates apMAPK (Aplysia mitogen-activated protein kinase), resulting in its entry into the nucleus. Surprisingly, studies using recombinant proteins in vivo and in vitro indicate that apPKG directly phosphorylates the threonine moiety in the T-E-Y activation site of apMAPK when the -Y-site contains a phosphate. We used inhibitors of nitric oxide synthase, soluble guanyl cyclase, or PKG after nerve injury, and found that each prevented the appearance of the LTH. Moreover, blocking apPKG activation prevented the nuclear import of apMAPK. Consequently, the nitric oxide-PKG-MAPK pathway is a potential target for treatment of neuropathic pain.

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Retrograde transport of plasticity signals in Aplysia sensory neurons following axonal injury

Abstract: We thank A. Clatworthy, M. Dulin, and P. Illich for comments on an earlier version of this article, J. Pastore for preparing the figures, and N. Karin for use of cell culture facilities.

Cited by 62 publications

References 40 publications

Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Memory-Like Alterations inAplysiaAxons after Nerve Injury or Localized Depolarization

Rotational dynamics of cargos at pauses during axonal transport

A Neuronal Isoform of Protein Kinase G Couples Mitogen-Activated Protein Kinase Nuclear Import to Axotomy-Induced Long-Term Hyperexcitability inAplysiaSensory Neurons

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