Abstract
Commentary: Serotonin Receptor 2B Mediates Mechanical Hyperalgesia by Regulating Transient Receptor Potential Vanilloid 1
Highlights
Serotonin [5-hydroxytryptamine (5-HT)] is known as a neurotransmitter, which is involved in regulating transmission of nociceptive signals in central nerve system1. 5-HT is an inflammatory mediator, released from immune cells, platelets and epithelial cells in the peripheral tissues
We previously demonstrated that 5-HT-induced mechanical hyperalgesia is attributed to 5-HT2B activation[4]
In Isolectin B4 (IB4)-negative neurons, 5-HT-induced calcium signals were inhibited by removal of extracellular calcium; while only some of IB4-positive neurons were sensitive to calcium-free condition
Summary
Serotonin [5-hydroxytryptamine (5-HT)] is known as a neurotransmitter, which is involved in regulating transmission of nociceptive signals in central nerve system1. 5-HT is an inflammatory mediator, released from immune cells, platelets and epithelial cells in the peripheral tissues. Our recent article provided more detail mechanism that 5-HT2B mediates Gq/11-phospholipase Cβ (PLCβ)-protein kinase Cε (PKCε) pathway to control mechanical hyperalgesia in both IB4-negative and -positive neurons. Transient receptor potential vanilloid 1 (TRPV1) and 5-HT3 are regulated by 5-HT2B to participate in 5-HT-induced mechanical hyperalgesia. The distinct roles of IB4-negative and IB4-positive neurons in 5-HT-induced mechanical hyperalgesia
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