| Guillain-Barre syndrome (GBS) is the most common cause of acute flaccid paralysis and an autoimmune disorder of the peripheral nervous system characterized by the progressive weakness, usually symmetrical, evolving over a period of several days or more. The classical is also called acute inflammatory demyelinating polyneuropathy (AIDP) characterized by an immune-mediated demyelination and varying degrees of lymphocytic infiltration in pathologic techniques and decreased conductive velocity of motor and sensory nerve by electrophysiological examination. Until recently, a new type of GBS with the same clinical manifestation has been found with different electrophysiological and pathological characters, especially in North China. The axon of ventral roots and distal motor fibers appears wallerian-like degeneration with myelin sheath relatively preserved and less infiltration of inflammatory mononuclear cells. This pattern was termed as acute motor axonal neuropathy (AMAN) with a relatively severe clinical course and a poor recovery. The etiology and pathogenesis of the condition has not been established. In recent years, the association between AMAN and preceding campylobacter jejuni (Cj) infection has been noticed. Professor Li in our department isolated campylobacter jejuni with O serotyping O:19 from an AMAN patient and developed an animal model of AMAN using this Cj strains with O serotyping O:19 and one of Cj structure-lipopolysaccharide (LPS). Anti-Cj or LPS antibodies were also found in the serum from AMAN patients. Plasmapheresis and intravenous human immunoglobulin administration are effective to lower the patient fatality, indicating some pathogenetic factor(s) exist in the circulation of AMAN patients and play an important role in the etiology and pathogenesis, even treatment in the AMAN. AMAN is an autoimmune disorder of theperipheral nervous system and the target of immune attack is axon of motor nerve. How the immune factors exert the damage is unclear, but the host immune system also play an even more important role in the developing AMAN. In some studies, complement C3d was found existing on the node of Ranvier using immunostain and complement activation presented in the periaxonal space, electron micrograph showing a macrophage surrounding the motor axon in patient with AMAN form of GBS. We established primary dissociated spinal motor neuron culture from embryonic rat to investigate the pathogenesis of AMAN. This culture system may take advantage in observing the axon damage from AMAN serum due to no limphocytes, mononuclear cells and complements exited which could not be eliminated in vivo and the axon-like neuritis extended from motor neurons without myelin out. Neuron is difficult to survive in vitro in dissociated cell culture because it is a kind of cell with high degree of differentiation and has soma and neuritis, especially for spinal motor neurons (SMNs) that are sensitive to environment and need nutrition as the lowest motor neurons. So in the first two parts, we established the SMNs dissociated culture in vitro and compared the influence of different substrates coated and a kind of neurotrophin-glial cell line-derived neurotrophic factor (GDNF) on the growth condition of SMNs, the third part is to investigate the effect of AMAN serum on the SMNs cultured.Part â… Influence of different substrate coated on spinal motor neurons cultured from embryonic ratsObjective: To isolate and incubate spinal motor neurons from embryonic rat and identify motor neurons in the culture firstly to develop the primary SMNs dissociated cell culture, then observe the influence of poly-L-lysine (PLL) dissolved in different solution on the growth of SMNs, and last to investigate the effect of different substrates coated including PLL, collagenâ… , laminin and PLL combined with laminin on the cell survival and neurite outgrowth of SMNs. Methods: The spinal cords were carefully isolated aseptically from embryo of pregnant 15 days Sprague-Dawley rat with all the roots and meninges dis... |
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