Cyclic AMP elevates tubulin expression without increasing intrinsic axon growth capacity

Han, Paul J.; Shukla, Salil; Subramanian, Prem S.; Hoffman, Paul N.

doi:10.1016/j.expneurol.2004.03.010

Cited by 51 publications

(37 citation statements)

References 60 publications

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“…results) is consistent with the long-term axonal regrowth process in this species (Lang et al, 2002(Lang et al, , 2008. Implication of cAMP in the upregulation of beta-III tubulin is a possibility to be explored in our material, as detected in the regenerating DRG neurons (Han et al, 2004). We may reasonably assume that damaged RGCs increase the biosynthesis of beta-III tubulin and HuCD, as regenerating neurons do in several vertebrates (Table 3).…”

Section: Neurons Synapses and Gs In Visual Systemsupporting

confidence: 82%

“…Neuronal microtubules are composed of alpha-and betatubulin heterodimers, which are found in numerous isotypes. Among them, the alpha-I, beta-II, and beta-III tubulin play a key role in axonal outgrowth after peripheral nerve injury in mammals (Miller et al, 1989;Moskowitz and Oblinger, 1995;Hoffman and Luduena, 1996;Han et al, 2004) and after ON injury in fish and mammals (Fournier and McKerracher, 1997;Hieber et al, 1998). We found that the selection of the beta-III tubulin was interesting for the current study since it is the most highly conserved among the different vertebrates species and appears to be expressed almost exclusively by neurons (review in Katsetos et al, 2003).…”

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confidence: 87%

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Expression of neuronal markers, synaptic proteins, and glutamine synthetase in the control and regenerating lizard visual system

Romero-Aleman

Monzon-Mayor

Santos

et al. 2010

J of Comparative Neurology

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Spontaneous regrowth of retinal ganglion cell (RGC) axons occurs after optic nerve (ON) transection in the lizard Gallotia galloti. To gain more insight into this event we performed an immunohistochemical study on selected neuron and glial markers, which proved useful for analyzing the axonal regrowth process in different regeneration models. In the control lizards, RGCs were beta-III tubulin- (Tuj1) and HuCD-positive. The vesicular glutamate transporter-1 (VGLUT1) preferentially stained RGCs and glial somata rather than synaptic layers. In contrast, SV2 and vesicular GABA/glycine transporter (VGAT) labeling was restricted to both plexiform layers. Strikingly, the strong expression of glutamine synthetase (GS) in both Müller glia processes and macroglial somata revealed a high glutamate metabolism along the visual system. Upregulation of Tuj1 and HuCD in the surviving RGCs was observed at all the timepoints studied (1, 3, 6, 9, and 12 months postlesion). The significant rise of Tuj1 in the optic nerve head and optic tract (OTr) by 1 and 6 months postlesion, respectively, suggests an increase of the beta-III tubulin transport and incorporation into newly formed axons. Persistent Tuj1(+) and SV2(+) puncta and swellings were abnormally observed in putative degenerating/dystrophic fibers. Unexpectedly, neuron-like cells of obscure significance were identified in the control and regenerating ON-OTr. We conclude that: 1) the persistent upregulation of Tuj1 and HuCD favors the long-lasting axonal regrowth process; 2) the latter succeeded despite the ectopia and dystrophy of some regrowing fibers; and 3) maintenance of the glutamate-glutamine cycle contributes to the homeostasis and plasticity of the system.

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Section: Neurons Synapses and Gs In Visual Systemsupporting

confidence: 82%

mentioning

confidence: 87%

Expression of neuronal markers, synaptic proteins, and glutamine synthetase in the control and regenerating lizard visual system

Romero-Aleman

Monzon-Mayor

Santos

et al. 2010

J of Comparative Neurology

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“…There is evidence that preconditioned regenerating sensory neurons develop an enhanced capacity for protein synthesis locally within the newly forming axon (Zheng et al, 2001;Brittis et al, 2002;Steward and Schuman, 2003). It may take considerable time for local synthetic machinery to reach sufficient levels to rapidly stimulate the production of an adequate repertoire of integrin receptors (Condic, 2001;Ekstrom et al, 2003;Irvins et al, 2004) or cytoskeletal elements (Zheng et al, 2001;Han et al, 2004) needed to allow the regenerating growth cone to move quickly from one substrate to another at the DREZ, avoiding turning or becoming dystrophic (Tom et al, 2004a). If we can elucidate the critical factors for axonal regrowth that are present after protracted conditioning, we may be able to enhance them more efficiently and, with matrix modification via ChABC, promote a more vigorous regeneration response after injury.…”

Section: Discussionmentioning

confidence: 99%

Chronic Enhancement of the Intrinsic Growth Capacity of Sensory Neurons Combined with the Degradation of Inhibitory Proteoglycans Allows Functional Regeneration of Sensory Axons through the Dorsal Root Entry Zone in the Mammalian Spinal Cord

et al. 2005

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Peripherally conditioned sensory neurons have an increased capacity to regenerate their central processes. However, even conditioned axons struggle in the presence of a hostile CNS environment. We hypothesized that combining an aggressive conditioning strategy with modification of inhibitory reactive astroglial-associated extracellular matrix could enhance regeneration. We screened potential treatments using a model of the dorsal root entry zone (DREZ). In this assay, a gradient of inhibitory chondroitin sulfate proteoglycans (CSPGs) stimulates formation of dystrophic end bulbs on adult sensory axons, which mimics regeneration failure in vivo. Combining inflammation-induced preconditioning of dorsal root ganglia in vivo before harvest, with chondroitinase ABC (ChABC) digestion of proteoglycans in vitro allows for significant regeneration across a once potently inhibitory substrate. We then assessed regeneration through the DREZ after root crush in adult rats receiving the combination treatment, ChABC, or zymosan pretreatment alone or no treatment. Regeneration was never observed in untreated animals, and only minimal regeneration occurred in the ChABC-and zymosanalone groups. However, remarkable regeneration was observed in a majority of animals that received the combination treatment. Regenerated fibers established functional synapses, as demonstrated electrophysiologically by the presence of an H-reflex. Two different postlesion treatment paradigms in which the timing of both zymosan and ChABC administration were varied after injury were ineffective in promoting regeneration. Therefore, zymosan pretreatment, but not posttreatment, of the sensory ganglia, combined with ChABC modification of CSPGs, resulted in robust and functional regeneration of sensory axons through the DREZ after root injury.

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“…Ca 2+ triggers a new life at fertilization, and controls the development and differentiation of the cells into specialized types, but it is also involved in cell death in a well defined cellular context. [48][49][50] Similar modulating effects on cell life and death may also be exercised by IP 3 , cAMP, ATP [51][52][53][54][55][56][57][58][59][60][61] .…”

Section: Introductionmentioning

confidence: 99%

Gap junctions and the propagation of cell survival and cell death signals

et al. 2005

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Gap junctions are a unique type of intercellular channels that connect the cytoplasm of adjoining cells. Each gap junction channel is comprised of two hemichannels or connexons and each connexon is formed by the aggregation of six protein subunits known as connexins. Gap junction channels allow the intercellular passage of small (< 1.5 kDa) molecules and regulate essential processes during development and differentiation. However, their role in cell survival and cell death is poorly understood. We review experimental data that support the hypothesis that gap junction channels may propagate cell death and survival modulating signals. In addition, we explore the hypothesis that hemichannels (or unapposed connexons) might be used as a paracrine conduit to spread factors that modulate the fate of the surrounding cells. Finally, direct signal transduction activity of connexins in cell death and survival pathways is addressed.

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Cyclic AMP elevates tubulin expression without increasing intrinsic axon growth capacity

Cited by 51 publications

References 60 publications

Expression of neuronal markers, synaptic proteins, and glutamine synthetase in the control and regenerating lizard visual system

Expression of neuronal markers, synaptic proteins, and glutamine synthetase in the control and regenerating lizard visual system

Chronic Enhancement of the Intrinsic Growth Capacity of Sensory Neurons Combined with the Degradation of Inhibitory Proteoglycans Allows Functional Regeneration of Sensory Axons through the Dorsal Root Entry Zone in the Mammalian Spinal Cord

Gap junctions and the propagation of cell survival and cell death signals

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