Development of a sensory afferent projection in the grasshopper embryo

Development ◽  
1981 ◽  
Vol 64 (1) ◽  
pp. 169-185
Author(s):  
Marty Shankland
Keyword(s):  
Sensory Neurons ◽  
Secondary Growth ◽  
Leading Edge ◽  
Growth Cones ◽  
Peripheral Neurons ◽  
Sensory Axons ◽  
Terminal Filament ◽  
Pioneer Neurons ◽  
Embryonic Cns ◽  
Prolonged Absence

The grasshopper's cereal nerve is established early in embryogenesis by an identified pair of peripheral neurons called the cereal pioneers. Like the peripheral pioneer neurons in other insect appendages, these two cells send their axons from the periphery to the rudimentary CNS and thus lay the foundation for a nerve that will later be followed by a large number of sensory axons. In this paper, cobalt fills of the primordial cereal nerve were used to characterize the disposition of these peripheral pioneer axons within the embryonic CNS. The pioneer axons stained by this technique terminate in ellipsoidal growth cones which have filopodia radiating from the leading edge and a single long terminal filament pointing along the path the axon is taking. The growing axons also bear filopodia along their sides, but these structures disappear as the cells mature. The pioneer axons of the cereal nerve make an abrupt turn where they first enter the ganglion rudiment and join the axons of the primary longitudinal tract. The pioneers then grow along this tract for several hundred microns without forming secondary growth cones or branches. This prolonged absence of central arborization distinguishes the peripheral pioneer axons from the axons of later-arising epidermal sensory neurons.

Glia dictate pioneer axon trajectories in the Drosophila embryonic CNS

Development ◽  
2000 ◽  
Vol 127 (2) ◽  
pp. 393-402 ◽  
Author(s):  
A. Hidalgo ◽  
G.E. Booth
Keyword(s):  
Axon Guidance ◽  
Molecular Mechanisms ◽  
Neuronal Cell ◽  
Cell Types ◽  
Growth Cones ◽  
Neuronal Cell Bodies ◽  
Direct Formation ◽  
Pioneer Neurons ◽  
Embryonic Cns ◽  
Made In

Whereas considerable progress has been made in understanding the molecular mechanisms of axon guidance across the midline, it is still unclear how the axonal trajectories of longitudinal pioneer neurons, which never cross the midline, are established. Here we show that longitudinal glia of the embryonic Drosophila CNS direct formation of pioneer axon pathways. By ablation and analysis of glial cells missing mutants, we demonstrate that glia are required for two kinds of processes. Firstly, glia are required for growth cone guidance, although this requirement is not absolute. We show that the route of extending growth cones is rich in neuronal cell bodies and glia, and also in long processes from both these cell types. Interactions between neurons, glia and their long processes orient extending growth cones. Secondly, glia direct the fasciculation and defasciculation of axons, which pattern the pioneer pathways. Together these events are essential for the selective fasciculation of follower axons along the longitudinal pathways.

Axon repulsion during peripheral nerve segmentation

Development ◽  
1991 ◽  
Vol 113 (Supplement_2) ◽  
pp. 131-139 ◽  
Author(s):  
Roger J. Keynes ◽  
Karen F. Jaques ◽  
Geoffrey M. W. Cook
Keyword(s):  
Dorsal Root ◽  
Grey Matter ◽  
Growth Cones ◽  
Spinal Nerve ◽  
Chick Embryos ◽  
Posterior Half ◽  
Similar Activity ◽  
Sensory Axons ◽  
Axon Repulsion

The guidance of axons during embryonic development is likely to involve both adhesive and repulsive interactions between growth cones and their environment. We are characterising the role and mechanism of repulsion during the segmental outgrowth of motor and sensory axons in the somite mesoderm of chick embryos. Axons are confined to the anterior half of each somite by the expression in the posterior half of a glycoconjugate system (48×103Mr and 55×103Mr) that causes the collapse of dorsal root ganglion growth cones when applied in vitro. Enzymatic cleavage of this fraction with specific combinations of endo- and exoglycosidases removes collapse activity, suggesting that carbohydrate residues are involved in the execution of collapse. A similar activity is also detectable in normal adult grey matter, suggesting roles for repulsion beyond the development of spinal nerve segmentation.

Immune-mediated alterations in nociceptive sensory function in Aplysia californica

1999 ◽  
Vol 202 (5) ◽  
pp. 623-630 ◽  
Author(s):  
A.L. Clatworthy ◽  
E. Grose
Keyword(s):  
Sensory Neurons ◽  
Interleukin 1 ◽  
Aplysia Californica ◽  
Sensory Function ◽  
Sensory Cells ◽  
Cellular Defense ◽  
Sensory Axons ◽  
Sensory Plasticity ◽  
Immune Mediated ◽  
Necrosis Factor

Nerve injury in Aplysia californica is accompanied by a profound long-lasting enhancement of the excitability of nociceptive sensory neurons that have axons in injured nerves. It is likely that a variety of signals are involved in triggering this injury-induced sensory plasticity. The objective of the present study was to determine whether cells of the cellular defense system (hemocytes) play a role in the modulation of sensory excitability following injury. In support of such an idea, we have shown previously that the induction of a cellular defense reaction close to sensory axons is accompanied by an increase in the excitability of sensory neurons with axons close to responding hemocytes. Furthermore, in the present study, we verified that, following axonal crush, numerous hemocytes accumulate at the injured site on the nerve. Using a hemocyte/nervous system co-culture preparation, we found that there were no significant differences in the expression of injury-induced sensory plasticity between sensory neurons incubated in the presence or absence of hemocytes. To overcome some potential limitations of our co-culture preparation, we used the endotoxin lipopolysaccharide (LPS) as a tool to activate the hemocytes. Sensory cells incubated in the presence of LPS and hemocytes were significantly more excitable than sensory cells incubated in the presence of LPS alone. We speculate that the addition of LPS to the incubation medium containing hemocytes enhanced the release of hemocyte-derived cytokine-like factors such as interleukin-1 and tumor necrosis factor. These cytokine-like factors may act as signals to modulate the expression of injury-induced sensory hyperexcitability.

Commissure formation in the embryonic CNS of Drosophila

Development ◽  
1999 ◽  
Vol 126 (4) ◽  
pp. 771-779 ◽  
Author(s):  
T. Hummel ◽  
K. Schimmelpfeng ◽  
C. Klambt
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Ventral Nerve Cord ◽  
Growth Cones ◽  
Cellular Functions ◽  
Detailed Model ◽  
Present Evidence ◽  
Embryonic Nervous System ◽  
Dependent Signal ◽  
Embryonic Cns

Most of the neurons of the ventral nerve cord send out long projecting axons which cross the midline. In the Drosophila central nervous system (CNS) cells of the midline give rise to neuronal and glial lineages with different functions during the establishment of the commissural pattern. Here we present evidence that beside the previously known NETRIN/FRAZZLED (DCC) signalling system an additional attractive system(s) is operating in the developing embryonic nervous system of Drosophila. Attractive cues appear to be provided by the midline neurons. We show that the glial cells present repulsive signals to the previously described ROUNDABOUT receptor in addition to a permissive contact-dependent signal helping commissural growth cones across the midline. A novel repulsive component is encoded by the karussell gene. Furthermore the midline glial cells separate anterior and posterior commissures. By genetic criteria we demonstrate that some of the genes we have identified are acting in the midline glia whereas other genes are required in the midline neurons. The results lead to a detailed model relating different cellular functions to axonal patterning at the midline.

Targeted neuronal ablation: the role of pioneer neurons in guidance and fasciculation in the CNS of Drosophila

Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3253-3262 ◽  
Author(s):  
A. Hidalgo ◽  
A.H. Brand
Keyword(s):  
Temporal Profile ◽  
Pioneer Neurons ◽  
Longitudinal Axon ◽  
Pioneer Neuron ◽  
Embryonic Cns

Although pioneer neurons are the first to delineate the axon pathways, it is uncertain whether they have unique pathfinding abilities. As a first step in defining the role of pioneer neurons in the Drosophila embryonic CNS, we describe the temporal profile and trajectory of the axons of four pioneer neurons and show that they differ from previously published reports. We show, by targeted ablation of one, two, three or four pioneer neurons at a time, that (1) no single pioneer neuron is essential for axon tract formation, (2) the interaction between two pioneers is necessary for the establishment of each fascicle and (3) pioneer neurons function synergistically to establish the longitudinal axon tracts, to guide the fasciculation of follower neurons along specific fascicles and to prevent axons from crossing the midline.

Zebrafish semaphorin Z1a collapses specific growth cones and alters their pathway in vivo

Development ◽  
1998 ◽  
Vol 125 (7) ◽  
pp. 1275-1283 ◽  
Author(s):  
W. Shoji ◽  
C.S. Yee ◽  
J.Y. Kuwada
Keyword(s):  
Sensory Neurons ◽  
Lateral Line ◽  
Knockout Mice ◽  
Specific Growth ◽  
Transmembrane Proteins ◽  
Growth Cones ◽  
In Vitro Activity ◽  
Different Strains

The semaphorin/collapsin gene family encodes secreted and transmembrane proteins several of which can repulse growth cones. Although the in vitro activity of Semaphorin III/D/Collapsin 1 is clear, recent analyses of two different strains of semaphorin III/D/collapsin 1 knockout mice have generated conflicting findings. In order to clarify the in vivo action of this molecule, we analyzed sema Z1a, a zebrafish homolog of semaphorin III/D/collapsin 1. The expression pattern of sema Z1a suggested that it delimited the pathway of the growth cones of a specific set of sensory neurons, the posterior ganglion of the lateral line, in zebrafish. To examine the in vivo action of this molecule, we analyzed (1) the pathways followed by lateral line growth cones in mutants in which the expression of sema Z1a is altered in an interesting way, (2) response of lateral line growth cones to exogenous Sema Z1a in living embryos, and (3) the pathway followed by lateral line growth cones when Sema Z1a is misexpressed by cells along their normal route. The results suggest that a repulsive action of Sema Z1a helps guide the growth cones of the lateral line along their normal pathway.

scholarly journals Shootin1–cortactin interaction mediates signal–force transduction for axon outgrowth

2015 ◽  
Vol 210 (4) ◽  
pp. 663-676 ◽  
Author(s):  
Yusuke Kubo ◽  
Kentarou Baba ◽  
Michinori Toriyama ◽  
Takunori Minegishi ◽  
Tadao Sugiura ◽  
...  
Keyword(s):  
Actin Polymerization ◽  
Leading Edge ◽  
Growth Cones ◽  
Axon Outgrowth ◽  
Actin Binding ◽  
Retrograde Flow ◽  
Environmental Chemical ◽  
Mechanical Coupling ◽  
Cell Adhesions ◽  
Force Transduction

Motile cells transduce environmental chemical signals into mechanical forces to achieve properly controlled migration. This signal–force transduction is thought to require regulated mechanical coupling between actin filaments (F-actins), which undergo retrograde flow at the cellular leading edge, and cell adhesions via linker “clutch” molecules. However, the molecular machinery mediating this regulatory coupling remains unclear. Here we show that the F-actin binding molecule cortactin directly interacts with a clutch molecule, shootin1, in axonal growth cones, thereby mediating the linkage between F-actin retrograde flow and cell adhesions through L1-CAM. Shootin1–cortactin interaction was enhanced by shootin1 phosphorylation by Pak1, which is activated by the axonal chemoattractant netrin-1. We provide evidence that shootin1–cortactin interaction participates in netrin-1–induced F-actin adhesion coupling and in the promotion of traction forces for axon outgrowth. Under cell signaling, this regulatory F-actin adhesion coupling in growth cones cooperates with actin polymerization for efficient cellular motility.

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