![]() ![]() 1, A and C, bars), and a control GFP adenovirus did not affect the AIS (Fig. The silencing of NF-186 did not reduce the number of neurons with NF-186 at the AIS ( Fig. Furthermore, they demonstrated that disruption of the actin-based cytoskeleton removed the AIS diffusion barrier and concluded that the AIS cytoskeleton regulates neuronal polarity. (1999) demonstrated that membrane proteins have different lateral mobilities in the AIS as compared with the distal axon. Given its unique molecular composition, location, and physiology, the AIS is thought to maintain neuronal polarity. It is responsible for action potential initiation and modulation ( Kole et al., 2007, 2008) and is highly enriched in ion channels, cell adhesion molecules (CAMs), and cytoskeletal and scaffolding proteins ( Hedstrom et al., 2007). The axon initial segment (AIS) functions as both a physical and physiological bridge between the somatodendritic and axonal domains. However, the molecular mechanisms maintaining neuronal polarity throughout life are unknown. Our results demonstrate that the loss of ankG causes axons to acquire the molecular characteristics of dendrites thus, ankG is required for the maintenance of neuronal polarity and molecular organization of the AIS.Īxon and dendrite specification during development (i.e., neuronal polarity) depends on positive and negative signals that regulate protein trafficking and cytoskeletal dynamics ( Arimura and Kaibuchi, 2007). Furthermore, spines and postsynaptic densities of excitatory synapses assemble on former axons. Both cytoplasmic- and membrane-associated proteins, which are normally restricted to somatodendritic domains, redistribute into the former axon. However, silencing the expression of the cytoskeletal scaffold ankyrinG (ankG) dismantles the AIS and causes axons to acquire the molecular characteristics of dendrites. Some AIS proteins are remarkably stable with half-lives of at least 2 wk. To identify the molecular basis of this AIS property, we used adenovirus-mediated RNA interference to silence AIS protein expression in polarized neurons. ![]() ![]() Phone: 001957 Fax: 000446 articles byĪddress correspondence to: Steven Petrou, Florey Neuroscience Institutes, The University of Melbourne, Parkville 3052, Victoria, Australia.The axon initial segment (AIS) functions as both a physiological and physical bridge between somatodendritic and axonal domains. 2The Centre for Neuroscience, The University of Melbourne, Parkville, Victoria, Australia.ģDepartment of Epileptology, University of Bonn Medical Center, Bonn, Germany.ĤHelmholtz-Institute for Radiation and Nuclear Physics andĥInterdisciplinary Center for Complex Systems, University of Bonn, Bonn, Germany.ĦNeurologische Klinik und Institut für Angewandte Physiologie der Universität Ulm, Zentrum Klinische Forschung, Ulm, Germany.ħAbteilung Neurologie mit Schwerpunkt Epileptologie, Hertie-Institut für klinische Hirnforschung, Universitätsklinikum Tübingen, Tübingen, Germany.ĨEpilepsy Research Centre, The University of Melbourne, Austin Health, Heidelberg West, Victoria, Australia.Īddress correspondence to: Steven Petrou, Florey Neuroscience Institutes, The University of Melbourne, Parkville 3052, Victoria, Australia. ![]()
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