Serotoninergic pain modulation from the rostral ventromedial medulla (RVM) in chemotherapy‐induced neuropathy: The role of spinal 5‐HT3 receptors

2019 ◽  
Vol 51 (8) ◽  
pp. 1756-1769 ◽  
Author(s):  
José Tiago Costa‐Pereira ◽  
Paula Serrão ◽  
Isabel Martins ◽  
Isaura Tavares
Keyword(s):  
Pain Modulation ◽  
Rostral Ventromedial Medulla ◽  
Ventromedial Medulla

scholarly journals Differential modulation of neurons in the rostral ventromedial medulla by neurokinin-1 receptors

2012 ◽  
Vol 107 (4) ◽  
pp. 1210-1221 ◽  
Author(s):  
Thaddeus S. Brink ◽  
Cholawat Pacharinsak ◽  
Sergey G. Khasabov ◽  
Alvin J. Beitz ◽  
Donald A. Simone
Keyword(s):  
Rostral Ventromedial Medulla ◽  
Intraplantar Injection ◽  
Nociceptive Transmission ◽  
Descending Facilitation ◽  
Pain Transmission ◽  
Ventromedial Medulla ◽  
Neurokinin 1 ◽  
Excitatory Responses ◽  
Heat Hyperalgesia

The rostral ventromedial medulla (RVM) is part of descending circuitry that modulates nociceptive processing at the level of the spinal cord. RVM output can facilitate pain transmission under certain conditions such as inflammation, and thereby contribute to hyperalgesia. Evidence suggests that substance P and activation of neurokinin-1 (NK-1) receptors in the RVM are involved in descending facilitation of nociception. We showed previously that injection of NK-1 receptor antagonists into the RVM attenuated mechanical and heat hyperalgesia produced by intraplantar injection of capsaicin. Furthermore, intraplantar injection of capsaicin excited ON cells in the RVM and inhibited ongoing activity of OFF cells. In the present studies, we therefore examined changes in responses of RVM neurons to mechanical and heat stimuli after intraplantar injection of capsaicin and determined the role of NK-1 receptors by injecting a NK-1 receptor antagonist into the RVM prior to capsaicin. After capsaicin injection, excitatory responses of ON cells and inhibitory responses of OFF cells evoked by mechanical and heat stimuli applied to the injected, but not contralateral, paw were increased. Injection of the NK-1 antagonist L-733,060 did not alter evoked responses of ON or OFF cells but attenuated the capsaicin-evoked enhanced responses of ON cells to mechanical and heat stimuli with less of an effect on the enhanced inhibitory responses of OFF cells. These data support the notion that descending facilitation from RVM contributes to hyperalgesia and that NK-1 receptors, presumably located on ON cells, play an important role in initiating descending facilitation of nociceptive transmission.

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