Inflammatory Pain. Figure 1

Mechanisms for the initiation and maintenance of inflammatory pain. Inflammatory pain is initiated by activation of nociceptive sensory neurons by hot or cold thermal stimulation, by mechanical stimulation, or by inflammatory mediators as indicated. Depolarization of sensory nerve endings in the periphery generate action potentials that travel to the spinal cord, thus conveying the noxious information. Inflammatory mediators can also reduce the threshold of activation of nociceptive sensory neurons, thereby producing peripheral sensitization (see text). Maintaining sensitization occurs with a sustained inflammatory response and with an increase in transcription, resulting in enhanced expression of proteins that regulate the excitability of sensory neurons. (Abbreviations: Glu, glutamate; ATP, adenosine triphosphate; Bk, bradykinin; 5Ht, 5-hydroxytryptamine; PGs, prostaglandins; LPAs, lysophosphatidic acids; NGF, nerve growth factor; S1P, sphingosine 1-phosphate).