| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
Pregabalin (PGB) is used for the peripheral and central neuropathic pain. Its mechanisms are selective binding to the α2δ subunit of voltage-gated calcium channels and reduce excitatory eurotransmitter release. The central nucleus amygdala (CeA) is a kernel site for the enhanced nociception-emotion link in the chronic pain. The nociceptive information is conveyed to CeA via two pathways. One is thalamocortical pathway that the projections from the basolateral amygdala (BLA) and the other is spinoparabrachial pathway that convey nociceptive informations directly from the externalpart of the pontine lateral parabrachial nucleus (LPB). We compared the effects of PGB on these excitatory inputs using formalin-treated inflammatory pain model mice. PGB inhibits the BLA to CeA transmission, but not the LPB to CeA, through a mechanism involving reduced release probability, particularly in inflammation conditions. These rsults suggests that PGB in treating the cognito-affective aspect of pain.
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