scholarly journals Myosin II Activity Facilitates Microtubule Bundling in the Neuronal Growth Cone Neck

2008 ◽  
Vol 15 (1) ◽  
pp. 163-169 ◽  
Author(s):  
Dylan T. Burnette ◽  
Lin Ji ◽  
Andrew W. Schaefer ◽  
Nelson A. Medeiros ◽  
Gaudenz Danuser ◽  
...  
Keyword(s):  
Growth Cone ◽  
Myosin Ii ◽  
Neuronal Growth ◽  
Neuronal Growth Cone

scholarly journals Myosin 1c and myosin IIB serve opposing roles in lamellipodial dynamics of the neuronal growth cone

2002 ◽  
Vol 158 (7) ◽  
pp. 1207-1217 ◽  
Author(s):  
Thomas J. Diefenbach ◽  
Vaughan M. Latham ◽  
Dean Yimlamai ◽  
Canwen A. Liu ◽  
Ira M. Herman ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Neurite Outgrowth ◽  
Growth Cone ◽  
Dorsal Root ◽  
Myosin Ii ◽  
Growth Cones ◽  
Neuronal Growth ◽  
Rapid Reduction ◽  
Neuronal Growth Cone

The myosin family of motor proteins is implicated in mediating actin-based growth cone motility, but the roles of many myosins remain unclear. We previously implicated myosin 1c (M1c; formerly myosin Iβ) in the retention of lamellipodia (Wang et al., 1996). Here we address the role of myosin II (MII) in chick dorsal root ganglion neuronal growth cone motility and the contribution of M1c and MII to retrograde F-actin flow using chromophore-assisted laser inactivation (CALI). CALI of MII reduced neurite outgrowth and growth cone area by 25%, suggesting a role for MII in lamellipodial expansion. Micro-CALI of MII caused a rapid reduction in local lamellipodial protrusion in growth cones with no effects on filopodial dynamics. This is opposite to micro-CALI of M1c, which caused an increase in lamellipodial protrusion. We used fiduciary beads (Forscher et al., 1992) to observe retrograde F-actin flow during the acute loss of M1c or MII. Micro-CALI of M1c reduced retrograde bead flow by 76%, whereas micro-CALI of MII or the MIIB isoform did not. Thus, M1c and MIIB serve opposite and nonredundant roles in regulating lamellipodial dynamics, and M1c activity is specifically required for retrograde F-actin flow.

scholarly journals Neuronal Growth Cone Retraction Relies on Proneurotrophin Receptor Signaling Through Rac

2011 ◽  
Vol 4 (202) ◽  
pp. ra82-ra82 ◽  
Author(s):  
K. Deinhardt ◽  
T. Kim ◽  
D. S. Spellman ◽  
R. E. Mains ◽  
B. A. Eipper ◽  
...  
Keyword(s):  
Growth Cone ◽  
Receptor Signaling ◽  
Neuronal Growth ◽  
Neuronal Growth Cone

Ultra-short pulses to signal neuronal growth cone machinery

2007 ◽  
Author(s):  
Manoj Mathew ◽  
Ivan Amat-Roldan ◽  
Rosa Andres ◽  
Iain G. Cormack ◽  
David Artigas ◽  
...  
Keyword(s):  
Growth Cone ◽  
Neuronal Growth ◽  
Short Pulses ◽  
Neuronal Growth Cone

The neuronal growth cone as a specialized transduction system

BioEssays ◽  
1991 ◽  
Vol 13 (3) ◽  
pp. 127-134 ◽  
Author(s):  
Stephen M. Strittmatter ◽  
Mark C. Fishman
Keyword(s):  
Growth Cone ◽  
Neuronal Growth ◽  
Neuronal Growth Cone

scholarly journals Rapid Impact of Progesterone on the Neuronal Growth Cone

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3784-3795 ◽  
Author(s):  
Laura Olbrich ◽  
Lisa Wessel ◽  
Ajeesh Balakrishnan-Renuka ◽  
Marion Böing ◽  
Beate Brand-Saberi ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Growth Cone ◽  
Progesterone Receptors ◽  
Laser Scanning Microscopy ◽  
Axonal Outgrowth ◽  
Neuronal Growth ◽  
Drg Neurons ◽  
Progesterone Treatment ◽  
Neuronal Growth Cone ◽  
The Impact

In the last two decades, sensory neurons and Schwann cells in the dorsal root ganglia (DRG) were shown to express the rate-limiting enzyme of the steroid synthesis, cytochrome P450 side-chain cleavage enzyme (P450scc), as well as the key enzyme of progesterone synthesis, 3β-hydroxysteroid dehydrogenase (3β-HSD). Thus, it was well justified to consider that DRG neurons similarly are able to synthesize progesterone de novo from cholesterol. Because direct progesterone effects on axonal outgrowth in peripheral neurons have not been investigated up to now, the present study provides the first insights into the impact of exogenous progesterone on axonal outgrowth in DRG neurons. Our studies including microinjection and laser scanning microscopy demonstrate morphological changes especially in the neuronal growth cones after progesterone treatment. Furthermore, we were able to detect a distinctly enhanced motility only a few minutes after the start of progesterone treatment using time-lapse imaging. Investigation of the cytoskeletal distribution in the neuronal growth cone before, during, and after progesterone incubation revealed a rapid reorganization of actin filaments. To get a closer idea of the underlying receptor mechanisms, we further studied the expression of progesterone receptors in DRG neurons using RT-PCR and immunohistochemistry. Thus, we could demonstrate for the first time that classical progesterone receptor (PR) A and B and the recently described progesterone receptor membrane component 1 (PGRMC1) are expressed in DRG neurons. Antagonism of the classical progesterone receptors by mifepristone revealed that the observed progesterone effects are transmitted through PR-A and PR-B.

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