Sigma-1 receptor: A drug target for the modulation of neuroimmune and neuroglial interactions during chronic pain
Metadatos
Afficher la notice complèteAuteur
Ruiz Cantero, María del Carmen; González Cano, Rafael; Tejada, Miguel Ángel; Santos Caballero, Miriam; Perazzoli, Gloria; Nieto, Francisco; Cobos del Moral, Enrique JoséEditorial
ELSEVIER
Materia
Pain Endogenous opioid analgesia Neuroinflammation Macrophages Microglia Astrocyte
Date
2020Referencia bibliográfica
Ruiz-Cantero, M. C., González-Cano, R., Tejada, M. Á., Santos-Caballero, M., Perazzoli, G., Nieto, F. R., & Cobos, E. J. (2020). Sigma-1 receptor: A drug target for the modulation of neuroimmune and neuroglial interactions during chronic pain. Pharmacological research. [DOI: 10.1016/j.phrs.2020.105339]
Patrocinador
Training University Lecturers program (FPU) of the Spanish Ministry of Economy and Competitiveness (MINECO); Biomedical Research Institute, Hospital Clfnico Universitario in Valencia (INCLIVA); Spanish State Research Agency of MINECO SAF2016-80540-R PID2019-108691RB-100; Andalusian Regional Government CTS109; European CommissionRésumé
Immune and glial cells play a pivotal role in chronic pain. Therefore, it is possible that the pharmacological
modulation of neurotransmission from an exclusively neuronal perspective may not be enough for adequate pain
management, and the modulation of complex interactions between neurons and other cell types might be needed
for successful pain relief. In this article, we review the current scientific evidence for the modulatory effects of
sigma-1 receptors on communication between the immune and nervous systems during inflammation, as well as
the influence of this receptor on peripheral and central neuroinflammation. Several experimental models of
pathological pain are considered, including peripheral and central neuropathic pain, osteoarthritic, and cancer
pain. Sigma-1 receptor inhibition prevents peripheral (macrophage infiltration into the dorsal root ganglion) and
central (activation of microglia and astrocytes) neuroinflammation in several pain models, and enhances
immune-driven peripheral opioid analgesia during painful inflammation, maximizing the analgesic potential of
peripheral immune cells. Therefore, sigma-1 antagonists may constitute a new class of analgesics with an unprecedented mechanism of action and potential utility in several painful disorders.