scholarly journals Differential neurite outgrowth is required for axon specification by cultured hippocampal neurons

2012 ◽  
Vol 123 (6) ◽  
pp. 904-910 ◽  
Author(s):  
Hideaki Yamamoto ◽  
Takanori Demura ◽  
Mayu Morita ◽  
Gary A. Banker ◽  
Takashi Tanii ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Hippocampal Neurons ◽  
Axon Specification ◽  
Cultured Hippocampal Neurons

Serotonin (5-HT) regulates neurite outgrowth through 5-HT1Aand 5-HT7receptors in cultured hippocampal neurons

2014 ◽  
Vol 92 (8) ◽  
pp. 1000-1009 ◽  
Author(s):  
Paulina S. Rojas ◽  
David Neira ◽  
Mauricio Muñoz ◽  
Sergio Lavandero ◽  
Jenny L. Fiedler
Keyword(s):  
Neurite Outgrowth ◽  
Hippocampal Neurons ◽  
Cultured Hippocampal Neurons

scholarly journals Transport of PIP3 by GAKIN, a kinesin-3 family protein, regulates neuronal cell polarity

2006 ◽  
Vol 174 (3) ◽  
pp. 425-436 ◽  
Author(s):  
Kaori Horiguchi ◽  
Toshihiko Hanada ◽  
Yasuhisa Fukui ◽  
Athar H. Chishti
Keyword(s):  
Hippocampal Neurons ◽  
Neuronal Cell ◽  
Neuronal Polarity ◽  
Transport Activity ◽  
Phosphatidylinositol 3 Kinase ◽  
Interacting Protein ◽  
Family Protein ◽  
Axon Specification ◽  
Cultured Hippocampal Neurons

Phosphatidylinositol-(3,4,5)-trisphosphate (PIP3), a product of phosphatidylinositol 3-kinase, is an important second messenger implicated in signal transduction and membrane transport. In hippocampal neurons, the accumulation of PIP3 at the tip of neurite initiates the axon specification and neuronal polarity formation. We show that guanylate kinase–associated kinesin (GAKIN), a kinesin-like motor protein, directly interacts with a PIP3-interacting protein, PIP3BP, and mediates the transport of PIP3-containing vesicles. Recombinant GAKIN and PIP3BP form a complex on synthetic liposomes containing PIP3 and support the motility of the liposomes along microtubules in vitro. In PC12 cells and cultured hippocampal neurons, transport activity of GAKIN contributes to the accumulation of PIP3 at the tip of neurites. In hippocampal neurons, altered accumulation of PIP3 by overexpression of GAKIN constructs led to the loss of the axonally differentiated neurites. Together, these results suggest that, in neurons, the GAKIN–PIP3BP complex transports PIP3 to the neurite ends and regulates neuronal polarity formation.

Directional control of neurite outgrowth from cultured hippocampal neurons is modulated by the lectin concanavalin A

1992 ◽  
Vol 23 (4) ◽  
pp. 354-363 ◽  
Author(s):  
Lynne M. Farmer ◽  
J�rg Hagmann ◽  
Daniel Dagan ◽  
Andrew I. Matus ◽  
Irwin B. Levitan
Keyword(s):  
Neurite Outgrowth ◽  
Concanavalin A ◽  
Hippocampal Neurons ◽  
Directional Control ◽  
Cultured Hippocampal Neurons

scholarly journals Suppression of kinesin expression in cultured hippocampal neurons using antisense oligonucleotides.

1992 ◽  
Vol 117 (3) ◽  
pp. 595-606 ◽  
Author(s):  
A Ferreira ◽  
J Niclas ◽  
R D Vale ◽  
G Banker ◽  
K S Kosik
Keyword(s):  
Neurite Outgrowth ◽  
Cell Body ◽  
Heavy Chain ◽  
Antisense Oligonucleotides ◽  
Hippocampal Neurons ◽  
Full Recovery ◽  
Synapsin I ◽  
Neurite Length ◽  
Protein Levels ◽  
Cultured Hippocampal Neurons

Kinesin, a microtubule-based force-generating molecule, is thought to translocate organelles along microtubules. To examine the function of kinesin in neurons, we sought to suppress kinesin heavy chain (KHC) expression in cultured hippocampal neurons using antisense oligonucleotides and study the phenotype of these KHC "null" cells. Two different antisense oligonucleotides complementary to the KHC sequence reduced the protein levels of the heavy chain by greater than 95% within 24 h after application and produced identical phenotypes. After inhibition of KHC expression for 24 or 48 h, neurons extended an array of neurites often with one neurite longer than the others; however, the length of all these neurites was significantly reduced. Inhibition of KHC expression also altered the distribution of GAP-43 and synapsin I, two proteins thought to be transported in association with membranous organelles. These proteins, which are normally localized at the tips of growing neurites, were confined to the cell body in antisense-treated cells. Treatment of the cells with the corresponding sense oligonucleotides affected neither the distribution of GAP-43 and synapsin I, nor the length of neurites. A full recovery of neurite length occurred after removal of the antisense oligonucleotides from the medium. These data indicate that KHC plays a role in the anterograde translocation of vesicles containing GAP-43 and synapsin I. A deficiency in vesicle delivery may also explain the inhibition of neurite outgrowth. Despite the inhibition of KHC and the failure of GAP-43 and synapsin I to move out of the cell body, hippocampal neurons can extend processes and acquire as asymmetric morphology.

scholarly journals Amphiphysin I Antisense Oligonucleotides Inhibit Neurite Outgrowth in Cultured Hippocampal Neurons

1998 ◽  
Vol 18 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Olaf Mundigl ◽  
Gian-Carlo Ochoa ◽  
Carol David ◽  
Vladimir I. Slepnev ◽  
Alexander Kabanov ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Antisense Oligonucleotides ◽  
Hippocampal Neurons ◽  
Cultured Hippocampal Neurons
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