Abstract
Tissue injury is associated with inflammation and produces inflammatory pain. In animal models, inflammatory pain is normally produced by injection of irritative chemicals into the hindpaw or joint of animal. Inflammatory pain manifests as an expression of neuronal plasticity, which consists of peripheral sensitization (increased sensitivity of primary sensory neurons in the peripheral nervous system, PNS) and central sensitization (increased sensitivity of spinal dorsal horn and other neurons in the central nervous system, CNS). Activation of several protein kinases causes both forms of sensitization via posttranslational, translational, and transcriptional regulation. In particular, mitogen-activated protein kinase (MAPK), such as ERK and p38, is activated by inflammatory mediators in primary sensory and secondary order dorsal horn neurons and participates in the generation and maintenance of inflammatory pain. Development of specific MAPK inhibitors will open a new avenue to the pharmacological intervention of inflammatory pain.
Keywords: inflammatory pain, peripheral sensitization, central sensitization, erk/mapk, p38 mapk, dorsal root ganglion, spinal cord dorsal horn
Related Journals
Anti-Cancer Agents in Medicinal Chemistry
Current Bioactive Compounds
Current Drug Safety
Current Drug Targets
Current Medicinal Chemistry
Current Pharmaceutical Biotechnology
Central Nervous System Agents in Medicinal Chemistry
Letters in Drug Design & Discovery
Current Drug Discovery Technologies
Recent Advances in Anti-Infective Drug Discovery
Related Books
Medicinal Plants, Phytomedicines and Traditional Herbal Remedies for Drug Discovery and Development against COVID-19
Key Heterocyclic Cores for Smart Anticancer Drug–Design Part II
Key Heterocyclic Cores for Smart Anticancer Drug–Design Part I
Frontiers in Cardiovascular Drug Discovery
Frontiers in Drug Design and Discovery
Frontiers in Anti-Cancer Drug Discovery
Frontiers in Drug Design and Discovery
Anti-Obesity Drug Discovery and Development
8