Activity-dependent postsynaptic receptor trafficking is critical for long-term synaptic plasticity in the brain, but it is unclear whether this mechanism actually mediates the spinal cord dorsal hom central sensitizat...Activity-dependent postsynaptic receptor trafficking is critical for long-term synaptic plasticity in the brain, but it is unclear whether this mechanism actually mediates the spinal cord dorsal hom central sensitization （a specific form of synaptic plasticity） that is associated with persistent pain. Recent studies have shown that peripheral inflammation drives changes in ct-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor （AMPAR） subunit trafficking in the dorsal horn and that such changes contribute to the hypersensitivity that underlies persistent pain. Here, we review current evi- dence to illustrate how spinal cord AMPARs participate in the dorsal hom central sensitization associated with persistent pain. Understanding these mechanisms may allow the development of novel therapeutic strategies for treating persistent pain.展开更多
Neuropeptide galanin is widespread in the nervous system and has been suggested to be involved in numerous neuronal and endocrine functions as an intercellular
Rice stripe virus(RSV)is the causative agent of rice stripe disease and is completely dependent on insect vectors for its plant-to-plant transmission.Laodelphax striatellus is the major insect vector for RSV.In this s...Rice stripe virus(RSV)is the causative agent of rice stripe disease and is completely dependent on insect vectors for its plant-to-plant transmission.Laodelphax striatellus is the major insect vector for RSV.In this study,we explored the interactions be-tween RSV infection and L.striatellus autophagy,a potential intrinsic antiviral mechanism in insects.We found that L.striatellus autophagic activity did not affect RSV infection;however,the autophagy related-8(Atg8)gene significantly enhanced virus infection.Dur-ing RSV initial infection within the L.striatellus midgut,silencing of Atg8 expression significantly decreased the phosphorylation of c-Jun N-terminal kinase(p-JNK);however,when RSV infection is absent,silencing of Atg8 did not alter p-JNK levels.Thesc results indicated that Atg8 might activate the JNK machinery by allowing more virus infection into cells.We further revealed that Atg8-deficiency significantly decreased RSV accumu-lation on the surface of the insect midgut epithelial cells,suggesting a receptor trafficking function of the y-aminobutyric acid receptor-associated protein family.Using the RSV ovary entry as a model,in which vitellogenin receptor(V gR)mediates RSV cell entry,we clarified that Atg8-deficiency decreased the abundance of V gR localizing on the cytomem-brane and disturbed the attachment of RSV in the germarium zones.Collectively,these results revealed an autophagy-independent function of L.striatellus Atg8 that enhances RSV initial infection by increasing virus attachment on the infection sites.展开更多
基金supported by grants from the National Institutes of Health (NS058886 and NS072206)Rita Allen Foundation+1 种基金Mr. David Koch and the Patrick C. Walsh Prostate Cancer Research Fundthe Blaustein Pain Research Fund
文摘Activity-dependent postsynaptic receptor trafficking is critical for long-term synaptic plasticity in the brain, but it is unclear whether this mechanism actually mediates the spinal cord dorsal hom central sensitization （a specific form of synaptic plasticity） that is associated with persistent pain. Recent studies have shown that peripheral inflammation drives changes in ct-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor （AMPAR） subunit trafficking in the dorsal horn and that such changes contribute to the hypersensitivity that underlies persistent pain. Here, we review current evi- dence to illustrate how spinal cord AMPARs participate in the dorsal hom central sensitization associated with persistent pain. Understanding these mechanisms may allow the development of novel therapeutic strategies for treating persistent pain.
文摘Neuropeptide galanin is widespread in the nervous system and has been suggested to be involved in numerous neuronal and endocrine functions as an intercellular
文摘Rice stripe virus(RSV)is the causative agent of rice stripe disease and is completely dependent on insect vectors for its plant-to-plant transmission.Laodelphax striatellus is the major insect vector for RSV.In this study,we explored the interactions be-tween RSV infection and L.striatellus autophagy,a potential intrinsic antiviral mechanism in insects.We found that L.striatellus autophagic activity did not affect RSV infection;however,the autophagy related-8(Atg8)gene significantly enhanced virus infection.Dur-ing RSV initial infection within the L.striatellus midgut,silencing of Atg8 expression significantly decreased the phosphorylation of c-Jun N-terminal kinase(p-JNK);however,when RSV infection is absent,silencing of Atg8 did not alter p-JNK levels.Thesc results indicated that Atg8 might activate the JNK machinery by allowing more virus infection into cells.We further revealed that Atg8-deficiency significantly decreased RSV accumu-lation on the surface of the insect midgut epithelial cells,suggesting a receptor trafficking function of the y-aminobutyric acid receptor-associated protein family.Using the RSV ovary entry as a model,in which vitellogenin receptor(V gR)mediates RSV cell entry,we clarified that Atg8-deficiency decreased the abundance of V gR localizing on the cytomem-brane and disturbed the attachment of RSV in the germarium zones.Collectively,these results revealed an autophagy-independent function of L.striatellus Atg8 that enhances RSV initial infection by increasing virus attachment on the infection sites.
