Pain

Pain refers to a complex sensory and emotional experience associated with actual or potential tissue damage[3][6]. It is mediated by specialized sensory neurons known as nociceptors, which detect noxious (harmful) mechanical, thermal, or chemical stimuli and transduce them into electrical signals transmitted to the central nervous system for interpretation as pain[2][3][6]. Pain is not a discrete molecule or biological receptor, but is perceived through the coordinated activity of various receptors, ion channels, and neurotransmitters at both peripheral and central levels. Examples of major molecular targets involved in pain perception and modulation include: - Voltage-gated sodium channels (e.g. Nav1.7/SCN9A, Nav1.8/SCN10A)[4][8] - Voltage-gated calcium channels[2][4] - Transient receptor potential (TRP) channels (e.g. TRPV1, TRPM8, TRPA1)[1][7] - Acid-sensing ion channels (ASICs)[6] - Purinergic receptors (e.g. P2X3)[1][2] - Opioid receptors (e.g. μ-opioid receptor)[6] - Neurotrophin receptors (e.g. NTRK1/TrkA)[1][8] - Cannabinoid receptors (e.g. CB1)[4] - Other neurotransmitter receptors and modulators (substance P, CGRP, GABA/Glutamate receptors, etc.)[1][2][6] Drugs acting on pain pathways include sodium channel blockers (e.g. lidocaine, carbamazepine), calcium channel blockers (e.g. gabapentin, pregabalin), TRP channel modulators (e.g. capsaicin), opioid receptor agonists (e.g. morphine), and non-steroidal anti-inflammatory drugs (NSAIDs), among others[2][6]. In summary, Pain is not a molecular target. For structured data relevant to pharmacological targeting, the specific molecule/receptor/channels (e.g. "Sodium channel protein type 9 subunit alpha" (Nav1.7/SCN9A), "Transient receptor potential cation channel subfamily V member 1" (TRPV1), "μ-opioid receptor") should be used instead.

Other names

N/Anociception

Drugs act on specific molecular targets and processes mediating pain sensation and transmission, including voltage-gated ion channels, TRP channels, and neurotransmitter receptors.