scholarly journals Beta 8 integrins mediate interactions of chick sensory neurons with laminin-1, collagen IV, and fibronectin.

1995 ◽  
Vol 6 (4) ◽  
pp. 419-431 ◽  
Author(s):  
K Venstrom ◽  
L Reichardt
Keyword(s):  
Neurite Outgrowth ◽  
Sensory Neurons ◽  
Binding Sites ◽  
Dorsal Root ◽  
Collagen Iv ◽  
Extracellular Matrices ◽  
Carboxyl Terminal ◽  
Dorsal Root Ganglia Neurons ◽  
Extracellular Matrix Receptors ◽  
Laminin 1

Integrins are major receptors used by cells to interact with extracellular matrices. In this paper, we identify the first ligands for the beta 8 family of integrins, presenting evidence that integrin heterodimers containing the beta 8 subunit mediate interactions of chick sensory neurons with laminin-1, collagen IV, and fibronectin. A polyclonal antibody, anti-beta 8-Ex, was prepared to a bacterial fusion protein expressing an extracellular portion of the chicken beta 8 subunit. In nonreducing conditions, this antibody immunoprecipitated from surface-labeled embryonic dorsal root ganglia neurons a M(r) 100 k protein, the expected M(r) of the beta 8 subunit, and putative alpha subunit(s) of M(r) 120 k. Affinity-purified anti-beta 8-Ex strongly inhibited sensory neurite outgrowth on laminin-1, collagen IV, and fibronectin-coated substrata. Binding sites were identified in a heat-resistant domain in laminin-1 and in the carboxyl terminal, 40-kDa fibronectin fragment. On substrates coated with the carboxyl terminal fragment of fibronectin, antibodies to beta 1 and beta 8 were only partially effective alone, but were completely effective in combination, at inhibiting neurite outgrowth. Results thus indicate that the integrin beta 8 subunit in association with one or more alpha subunits forms an important set of extracellular matrix receptors on sensory neurons.

scholarly journals Expression of beta 1 integrins in sensory neurons of the dorsal root ganglion and their functions in neurite outgrowth on two laminin isoforms

1993 ◽  
Vol 13 (11) ◽  
pp. 4880-4888 ◽  
Author(s):  
KJ Tomaselli ◽  
P Doherty ◽  
CJ Emmett ◽  
CH Damsky ◽  
FS Walsh ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Neurite Outgrowth ◽  
Sensory Neurons ◽  
Dorsal Root

pp60 Is a Negative Regulator of Laminin-1-Mediated Neurite Outgrowth in Chick Sensory Neurons

2002 ◽  
Vol 21 (1) ◽  
pp. 81-93 ◽  
Author(s):  
Diane Hoffman-Kim ◽  
Julie A. Kerner ◽  
Andrew Chen ◽  
Alian Xu ◽  
Ting-Fang Wang ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Sensory Neurons ◽  
Negative Regulator ◽  
Laminin 1

scholarly journals Neurite outgrowth on immobilized axonin-1 is mediated by a heterophilic interaction with L1(G4).

1991 ◽  
Vol 115 (4) ◽  
pp. 1113-1126 ◽  
Author(s):  
T B Kuhn ◽  
E T Stoeckli ◽  
M A Condrau ◽  
F G Rathjen ◽  
P Sonderegger
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Dorsal Root Ganglia ◽  
Adhesion Molecule ◽  
Dorsal Root ◽  
Cell Adhesion Molecule ◽  
Neurite Growth ◽  
Soluble Form ◽  
Axonal Membrane ◽  
Dorsal Root Ganglia Neurons

Axonin-1 is an axon-associated cell adhesion molecule with dualistic expression, one form being glycophosphatidylinositol-anchored to the axonal membrane, the other secreted from axons in a soluble form. When presented as a substratum for neuronal cultures it strongly promotes neurite outgrowth from chicken embryonic dorsal root ganglia neurons. In this study, the axon-associated cell adhesion molecule G4, which is identical with Ng-CAM and 8D9, and homologous or closely related to L1 of the mouse and NILE of the rat, was investigated with respect to a receptor function for axonin-1. Using fluorescent microspheres with covalently coupled axonin-1 or L1(G4) at their surface we showed that these proteins bind to each other. Within the sensitivity of this microsphere assay, no interaction of axonin-1 with itself could be detected. Axonin-1-coated microspheres also bound to the neurites of cultured dorsal root ganglia neurons. This interaction was exclusively mediated by L1(G4), as indicated by complete binding suppression by monovalent anti-L1(G4) antibodies. The interaction between neuritic L1(G4) and immobilized axonin-1 was found to mediate the promotion of neurite growth on axonin-1, as evidenced by the virtually complete arrest of neurite outgrowth in the presence of anti-L1(G4) antibodies. Convincing evidence has recently been presented that neurite growth on L1(8D9) is mediated by the homophilic binding of neuritic L1(G4) (1989. Neuron. 2: 1597-1603). Thus, both L1(G4)- and axonin-1-expressing axons may serve as "substrate pathways" for the guidance of following axons expressing L1(G4) into their target area. Conceivably, differences in the concentration of axonin-1 and L1(G4), and/or modulatory influences on their specific binding parameters in leading pathways and following axons could represent elements in the control of axonal pathway selection.

scholarly journals Cell adhesion molecules NgCAM and axonin-1 form heterodimers in the neuronal membrane and cooperate in neurite outgrowth promotion.

1996 ◽  
Vol 135 (6) ◽  
pp. 1593-1607 ◽  
Author(s):  
A Buchstaller ◽  
S Kunz ◽  
P Berger ◽  
B Kunz ◽  
U Ziegler ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Dorsal Root Ganglia ◽  
Growth Cone ◽  
Dorsal Root ◽  
Cell Aggregation ◽  
Neuronal Membrane ◽  
Direct Binding ◽  
Dorsal Root Ganglia Neurons ◽  
Cis Interaction

The axonal surface glycoproteins neuronglia cell adhesion molecule (NgCAM) and axonin-1 promote cell-cell adhesion, neurite outgrowth and fasciculation, and are involved in growth cone guidance. A direct binding between NgCAM and axonin-1 has been demonstrated using isolated molecules conjugated to the surface of fluorescent microspheres. By expressing NgCAM and axonin-1 in myeloma cells and performing cell aggregation assays, we found that NgCAM and axonin-1 cannot bind when present on the surface of different cells. In contrast, the cocapping of axonin-1 upon antibody-induced capping of NgCAM on the surface of CV-1 cells coexpressing NgCAM and axonin-1 and the selective chemical cross-linking of the two molecules in low density cultures of dorsal root ganglia neurons indicated a specific and direct binding of axonin-1 and Ng-CAM in the plane of the same membrane. Suppression of the axonin-1 translation by antisense oligonucleotides prevented neurite outgrowth in dissociated dorsal root ganglia neurons cultured on an NgCAM substratum, indicating that neurite outgrowth on NgCAM substratum requires axonin-1. Based on these and previous results, which implicated NgCAM as the neuronal receptor involved in neurite outgrowth on NgCAM substratum, we concluded that neurite outgrowth on an NgCAM substratum depends on two essential interactions of growth cone NgCAM: a trans-interaction with substratum NgCAM and a cis-interaction with axonin-1 residing in the same growth cone membrane.

Effects of anoxia, aglycemia, and acidosis on cytosolic Mg2+, ATP, and pH in rat sensory neurons

2008 ◽  
Vol 294 (1) ◽  
pp. C280-C294 ◽  
Author(s):  
Michael Henrich ◽  
Keith J. Buckler
Keyword(s):  
Cell Line ◽  
Intracellular Ph ◽  
Sensory Neurons ◽  
Dorsal Root Ganglia ◽  
Binding Sites ◽  
Dorsal Root ◽  
Metabolic Inhibition ◽  
Metabolic Challenge ◽  
Two Phases ◽  
Neuron Function

Sensory neurons can detect ischemia and transmit pain from various organs. Whereas the primary stimulus in ischemia is assumed to be acidosis, little is known about how the inevitable metabolic challenge influences neuron function. In this study we have investigated the effects of anoxia, aglycemia, and acidosis upon intracellular Mg2+ concentration [Mg2+]i and intracellular pH (pHi) in isolated sensory neurons. Anoxia, anoxic aglycemia, and acidosis all caused a rise in [Mg2+]i and a fall in pHi. The rise in [Mg2+]i in response to acidosis appears to be due to H+ competing for intracellular Mg2+ binding sites. The effects of anoxia and aglycemia were mimicked by metabolic inhibition and, in a dorsal root ganglia (DRG)-derived cell line, the rise in [Mg2+]i during metabolic blockade was closely correlated with fall in intracellular ATP concentration ([ATP]i). Increase in [Mg2+]i during anoxia and aglycemia were therefore assumed to be due to MgATP hydrolysis. Even brief periods of anoxia (<3 min) resulted in rapid internal acidosis and a rise in [Mg2+]i equivalent to a decline in MgATP levels of 15–20%. With more prolonged anoxia (20 min) MgATP depletion is estimated to be around 40%. With anoxic aglycemia, the [Mg2+]i rise occurs in two phases: the first beginning almost immediately and the second after an 8- to 10-min delay. Within 20 min of anoxic aglycemia [Mg2+]i was comparable to that observed following complete metabolic inhibition (dinitrophenol + 2-deoxyglucose, DNP + 2-DOG) indicating a near total loss of MgATP. The consequences of these events therefore need to be considered in the context of sensory neuron function in ischemia.

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