Abstract
Lysophosphatidic acid or LPA is a phospholipid which has been extensively linked to the generation and maintenance of pain. Several ion channels have also been shown to participate in this pathological process but the link between LPA and these proteins in pain has just recently gained interest. In this respect, the field has advanced by determining the molecular mechanisms by which LPA promotes changes in the function of some ion channels. While some of the actions of LPA include modulation of signaling pathways associated to its specific receptors, other include a direct interaction with a region in the structure of ion channels to affect their gating properties. Here, we focus on the known effects of LPA on some transient receptor potential, sodium, potassium, and calcium channels. As the field moves forward, mechanisms are unveiled with the hope of understanding the underlying causes of pain in order to target these and control this pathophysiological state.
Highlights
Nociceptors are peripheral sensory neurons that respond to a wide diversity of harmful stimuli and transduce these stimuli into signals that reach the brain (Dubin and Patapoutian, 2010), leading to the subjective experience of pain defined as an “unpleased sensory and emotional experience associated with actual or potential tissue damage” (International Association of Pain Study).Neuronal activity is initiated at these specialized neurons, with somas located at the dorsal root ganglia (DRG) or trigeminal ganglia (TG) (Dubin and Patapoutian, 2010)
Neuronal activity is initiated at these specialized neurons, with somas located at the dorsal root ganglia (DRG) or trigeminal ganglia (TG) (Dubin and Patapoutian, 2010)
We demonstrated that lysophosphatidic acid (LPA) elicited action potential firing in WT mouse DRGs, whereas this electrical activity was not observed in DRG neurons from TRPV1 KO mice
Summary
División de Neurociencias, Instituto de Fisiología Celular, Departamento de Neurociencia Cognitiva, Universidad Nacional Autónoma de México, Ciudad de México, Mexico. Several ion channels have been shown to participate in this pathological process but the link between LPA and these proteins in pain has just recently gained interest. In this respect, the field has advanced by determining the molecular mechanisms by which LPA promotes changes in the function of some ion channels. While some of the actions of LPA include modulation of signaling pathways associated to its specific receptors, other include a direct interaction with a region in the structure of ion channels to affect their gating properties. We focus on the known effects of LPA on some transient receptor potential, sodium, potassium, and calcium channels. As the field moves forward, mechanisms are unveiled with the hope of understanding the underlying causes of pain in order to target these and control this pathophysiological state
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