p75 Neurotrophin Receptor Signaling Regulates Growth Cone Filopodial Dynamics through Modulating RhoA Activity

Gehler, Scott; Gallo, Gianluca; Veien, Eric S.; Letourneau, Paul C.

doi:10.1523/jneurosci.0404-04.2004

Cited by 118 publications

(125 citation statements)

References 60 publications

(68 reference statements)

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“…S5, available at www.jneurosci.org as supplemental material) (Nagata-Ohashi et al, 2004). We confirmed that application of an NGF gradient results in an attractive mean turning angle when applied to E8 chick DRG growth cones (Gundersen and Barrett, 1980;Gehler et al, 2004) and we find that this response is unaffected by HSV-R18-GFP (12.6 Ϯ 5.8°; Fig. 2a,d).…”

Section: -3-3 Proteins Are Expressed In Neuronal Growth Conessupporting

confidence: 77%

14-3-3 Proteins Regulate Protein Kinase A Activity to Modulate Growth Cone Turning Responses

Kent¹,

Shimada²,

Ferraro³

et al. 2010

J. Neurosci.

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Growth cones regulate the speed and direction of neuronal outgrowth during development and regeneration. How the growth cone spatially and temporally regulates signals from guidance cues is poorly understood. Through a proteomic analysis of purified growth cones we identified isoforms of the 14-3-3 family of adaptor proteins as major constituents of the growth cone. Disruption of 14-3-3 via the R18 antagonist or knockdown of individual 14-3-3 isoforms switches nerve growth factor-and myelin-associated glycoproteindependent repulsion to attraction in embryonic day 13 chick and postnatal day 5 rat DRG neurons. These effects are reminiscent of switching responses observed in response to elevated cAMP. Intriguingly, R18-dependent switching is blocked by inhibitors of protein kinase A (PKA), suggesting that 14-3-3 proteins regulate PKA. Consistently, 14-3-3 proteins interact with PKA and R18 activates PKA by dissociating its regulatory and catalytic subunits. Thus, 14-3-3 heterodimers regulate the PKA holoenzyme and this activity plays a critical role in modulating neuronal responses to repellent cues.

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Section: -3-3 Proteins Are Expressed In Neuronal Growth Conessupporting

confidence: 77%

14-3-3 Proteins Regulate Protein Kinase A Activity to Modulate Growth Cone Turning Responses

Kent¹,

Shimada²,

Ferraro³

et al. 2010

J. Neurosci.

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“…However, it should be noted that GABA might not represent the only calcium generator because blocking GABA A receptor activity did not completely abolish lamellipodia activity and dendritic growth. Candidate molecules that could be involved in this process include neurotrophins (Gehler et al, 2004) and integrins (Bonner and O'Connor, 2001).…”

Section: Discussionmentioning

confidence: 99%

GABA Regulates Dendritic Growth by Stabilizing Lamellipodia in Newly Generated Interneurons of the Olfactory Bulb

Gascon¹,

Dayer²,

Sauvain³

et al. 2006

J. Neurosci.

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The initial formation and growth of dendrites is a critical step leading to the integration of newly generated neurons into postnatal functional networks. However, the cellular mechanisms and extracellular signals regulating this process remain mostly unknown. By directly observing newborn neurons derived from the subventricular zone in culture as well as in olfactory bulb slices, we show that ambient GABA acting through GABA A receptors is essential for the temporal stability of lamellipodial protrusions in dendritic growth cones but did not interfere with filopodia dynamics. Furthermore, we provide direct evidence that ambient GABA is required for the proper initiation and elongation of dendrites by promoting the rapid stabilization of new dendritic segments after their extension. The effects of GABA on the initial formation of dendrites depend on depolarization and Ca 2ϩ influx and are associated with a higher stability of microtubules. Together, our results indicate that ambient GABA is a key regulator of dendritic initiation in postnatally generated olfactory interneurons and offer a mechanism by which this neurotransmitter drives early dendritic growth.

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“…This expression pattern is critical for successful innervation of taste epithelia by gustatory neurons (Ringstedt et al, 1999;Krimm et al, 2001), suggesting that BDNF plays a chemotactic role during the final stages of axon targeting. The p75 receptor is also important for neurotrophin regulation of growth cone dynamics in vitro Gehler et al, 2004). It is possible that BDNF-mediated gustatory axon targeting is disrupted in p75 À/À mice.…”

Section: Discussionmentioning

confidence: 99%

“…For example, the p75 receptor has been shown to enhance neuron survival in some instances (Stucky and Koltzenburg, 1997;DeFreitas et al, 2001;Song and Posse de Chaves, 2003) and to mediate cell death in others (Agerman et al, 2000;Botchkarev et al, 2000;Lee et al, 2001;Troy et al, 2002). Axon growth (Yamashita et al, 1999;Bentley and Lee, 2000;Gallo and Letourneau, 2004;Gehler et al, 2004) and axonal regeneration (Boyd and Gordon, 2001;Song et al, 2004Song et al, , 2005Yamashita et al, 2005b) are also differentially regulated by this receptor.…”

mentioning

confidence: 99%

Mice lacking the p75 receptor fail to acquire a normal complement of taste buds and geniculate ganglion neurons by adulthood

Krimm

2006

Anat. Rec.

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Brain-derived neurotrophic factor and neurotrophin-4 are required for normal taste bud development. Although these neurotrophins normally function via the tyrosine kinase receptor, trkB, they also bind to the panneurotrophin receptor, p75. The goal of the present study was to determine whether the p75 receptor is required for the development or maintenance of a full complement of adult taste buds. Mice with p75 null mutations lose 34% of their circumvallate taste buds, 36% of their fungiform papillae, and 26% of their fungiform taste buds by adulthood. The reduction of taste buds in the adult circumvallate papilla was similar to that observed previously at postnatal day 7 (Fan et al. Brain Res Dev Brain Res 2004;150:23-39). Taken together, these findings indicate that the p75 receptor is critical for the development of a full complement of taste buds, but is not required for maintenance of circumvallate taste buds in adulthood. Immunolabeling for p75 was not observed in taste buds, indicating that p75 signaling influences taste bud number indirectly. Geniculate ganglion neurons, which provides innervation to fungiform taste buds, express the p75 receptor. Mice with p75 null mutations also have fewer neurons in the geniculate ganglion. Together, these results suggest that the p75 receptor is important for the survival of geniculate neurons and geniculate neuron survival is required for the development of a full complement of taste buds by adulthood.

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p75 Neurotrophin Receptor Signaling Regulates Growth Cone Filopodial Dynamics through Modulating RhoA Activity

Cited by 118 publications

References 60 publications

14-3-3 Proteins Regulate Protein Kinase A Activity to Modulate Growth Cone Turning Responses

14-3-3 Proteins Regulate Protein Kinase A Activity to Modulate Growth Cone Turning Responses

GABA Regulates Dendritic Growth by Stabilizing Lamellipodia in Newly Generated Interneurons of the Olfactory Bulb

Mice lacking the p75 receptor fail to acquire a normal complement of taste buds and geniculate ganglion neurons by adulthood

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