Transient receptor potential channel A1 is one of the important transducers of noxious stimuli in the primary afferents, which may contribute to generation of neurogenic inflammation and hyperalgesia. The present stud...Transient receptor potential channel A1 is one of the important transducers of noxious stimuli in the primary afferents, which may contribute to generation of neurogenic inflammation and hyperalgesia. The present study was designed to investigate if activation of transient receptor potential channel A1 may induce calcitonin gene-related peptide release from the primary afferent neurons. We found that application of allyl isothiocyanate, a transient receptor potential channel A1 activator, caused calcitonin gene-related peptide release from the cultured rat dorsal root ganglion neurons. Knock- down of transient receptor potential channel A1 with an antisense oligodeoxynucleotide prevented calcitonin gene-related peptide release by allyl isothiocyanate application in cultured dorsal root ganglion neurons. Thus, we concluded that transient receptor potential channel A1 activation caused calcitonin gene-related peptide release in sensory neurons.展开更多
Fluctuations in gene expression that reflect changes in the functional demands on individual neurons are an everyday occurrence. With sustained peripheral inflammation, however, prolonged C-fiber activation alters the...Fluctuations in gene expression that reflect changes in the functional demands on individual neurons are an everyday occurrence. With sustained peripheral inflammation, however, prolonged C-fiber activation alters the pattern of gene transcription in dorsal root ganglion (DRG) cells and dorsal horn neurons. Following peripheral nerve injury changes in neuronal excitability and mRNA levels in sensory neurons offer s substrate for chronic pain. Several mechanisms that contribute to increased excitability in DRG have recently been discovered.展开更多
基金supported by the Research Basis Formation Supporting Project for Private University
文摘Transient receptor potential channel A1 is one of the important transducers of noxious stimuli in the primary afferents, which may contribute to generation of neurogenic inflammation and hyperalgesia. The present study was designed to investigate if activation of transient receptor potential channel A1 may induce calcitonin gene-related peptide release from the primary afferent neurons. We found that application of allyl isothiocyanate, a transient receptor potential channel A1 activator, caused calcitonin gene-related peptide release from the cultured rat dorsal root ganglion neurons. Knock- down of transient receptor potential channel A1 with an antisense oligodeoxynucleotide prevented calcitonin gene-related peptide release by allyl isothiocyanate application in cultured dorsal root ganglion neurons. Thus, we concluded that transient receptor potential channel A1 activation caused calcitonin gene-related peptide release in sensory neurons.
文摘Fluctuations in gene expression that reflect changes in the functional demands on individual neurons are an everyday occurrence. With sustained peripheral inflammation, however, prolonged C-fiber activation alters the pattern of gene transcription in dorsal root ganglion (DRG) cells and dorsal horn neurons. Following peripheral nerve injury changes in neuronal excitability and mRNA levels in sensory neurons offer s substrate for chronic pain. Several mechanisms that contribute to increased excitability in DRG have recently been discovered.
