Cholecystokinin type B receptor-mediated inhibition of A-type K+ channels enhances sensory neuronal excitability through the phosphatidylinositol 3-kinase and c-Src-dependent JNK pathway.
Shumin YuYuan ZhangXianyang ZhaoZhigang ChangYuan WeiYufang SunDongsheng JiangXinghong JiangJin TaoPublished in: Cell communication and signaling : CCS (2019)
Our findings indicate that CCK-8 attenuated IA through CCK-BR that is coupled to the Gβγ-dependent PI3K and c-Src-mediated JNK pathways, thereby enhancing the sensory neuronal excitability in DRG neurons and peripheral pain sensitivity in mice.
Keyphrases
- tyrosine kinase
- signaling pathway
- cell death
- transcranial direct current stimulation
- chronic pain
- protein kinase
- induced apoptosis
- spinal cord
- cerebral ischemia
- pain management
- neuropathic pain
- type diabetes
- oxidative stress
- spinal cord injury
- metabolic syndrome
- skeletal muscle
- working memory
- endoplasmic reticulum stress
- wild type