scholarly journals The dynein inhibitor Ciliobrevin D inhibits the bidirectional transport of organelles along sensory axons and impairs NGF-mediated regulation of growth cones and axon branches

2014 ◽  
Vol 75 (7) ◽  
pp. 757-777 ◽  
Author(s):  
Rajiv Sainath ◽  
Gianluca Gallo
Development ◽  
1991 ◽  
Vol 113 (Supplement_2) ◽  
pp. 131-139 ◽  
Author(s):  
Roger J. Keynes ◽  
Karen F. Jaques ◽  
Geoffrey M. W. Cook

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.


2003 ◽  
Vol 89 (6) ◽  
pp. 3225-3234 ◽  
Author(s):  
Nidhi Rumpal ◽  
Gregory A. Lnenicka

Intracellular free Ca2+ concentration ([Ca2+]i) plays an important role in the regulation of growth cone (GC) motility; however, the mechanisms responsible for clearing Ca2+ from GCs have not been examined. We studied the Ca2+-clearance mechanisms in GCs produced by crayfish tonic and phasic motor axons by measuring the decay of [Ca2+]i after a high [K+] depolarizing pulse using fura-2AM. Tonic motor axons regenerating in explant cultures develop GCs with more rapid Ca2+ clearance than GCs from phasic axons. When Na/Ca exchange was blocked by replacing external Na+ with N-methyl-d-glucamine (NMG), [Ca2+]i decay was delayed in both tonic and phasic GCs. Tonic GCs appear to have higher Na/Ca exchange activity than phasic ones since reversal of Na/Ca exchange by lowering external Na+ caused a greater increase in [Ca2+]i for tonic than phasic GCs. Application of the mitochondrial inhibitors, Antimycin A1 (1 μM) and CCCP (10 μM), demonstrated that mitochondrial Ca2+ uptake/release was more prominent in phasic than tonic GCs. When both Na/Ca exchange and mitochondria were inhibited, the plasma membrane Ca2+ ATPase was effective in extruding Ca2+ from tonic, but not phasic GCs. We conclude that Na/Ca exchange plays a prominent role in extruding large Ca2+ loads from both tonic and phasic GCs. High Na/Ca exchange activity in tonic GCs contributes to the rapid decay of [Ca2+]i in these GCs; low rates of Ca2+ extrusion plus the release of Ca2+ from mitochondria prolongs the decay of [Ca2+]i in the phasic GCs.


1992 ◽  
Vol 572 (1-2) ◽  
pp. 139-145 ◽  
Author(s):  
Pär Remgård ◽  
Magnus Edbladh ◽  
Per A.R. Ekström ◽  
Anders Edström
Keyword(s):  

Development ◽  
1981 ◽  
Vol 64 (1) ◽  
pp. 169-185
Author(s):  
Marty Shankland

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.


2003 ◽  
Vol 89 (6) ◽  
pp. 3225-3234 ◽  
Author(s):  
Nidhi Rumpal ◽  
Gregory A. Lnenicka

Intracellular free Ca2+ concentration ([Ca2+]i) plays an important role in the regulation of growth cone (GC) motility; however, the mechanisms responsible for clearing Ca2+ from GCs have not been examined. We studied the Ca2+-clearance mechanisms in GCs produced by crayfish tonic and phasic motor axons by measuring the decay of [Ca2+]i after a high [K+] depolarizing pulse using fura-2AM. Tonic motor axons regenerating in explant cultures develop GCs with more rapid Ca2+ clearance than GCs from phasic axons. When Na/Ca exchange was blocked by replacing external Na+ with N-methyl-d-glucamine (NMG), [Ca2+]i decay was delayed in both tonic and phasic GCs. Tonic GCs appear to have higher Na/Ca exchange activity than phasic ones since reversal of Na/Ca exchange by lowering external Na+ caused a greater increase in [Ca2+]i for tonic than phasic GCs. Application of the mitochondrial inhibitors, Antimycin A1 (1 μM) and CCCP (10 μM), demonstrated that mitochondrial Ca2+ uptake/release was more prominent in phasic than tonic GCs. When both Na/Ca exchange and mitochondria were inhibited, the plasma membrane Ca2+ ATPase was effective in extruding Ca2+ from tonic, but not phasic GCs. We conclude that Na/Ca exchange plays a prominent role in extruding large Ca2+ loads from both tonic and phasic GCs. High Na/Ca exchange activity in tonic GCs contributes to the rapid decay of [Ca2+]i in these GCs; low rates of Ca2+ extrusion plus the release of Ca2+ from mitochondria prolongs the decay of [Ca2+]i in the phasic GCs.


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