Modulation of Pain by Endocannabinoids in the Periphery

Activation of cannabinoid receptors using systemic treatments produces analgesia in a variety of experimental pain models, but these effects are hindered by sedation and motor impairment mediated by receptors in the central nervous system. Targeting the endocannabinoid system in the periphery can bypass these unwanted side effects while still producing analgesia in both acute and chronic pain states. This chapter discusses the different approaches to increasing peripheral endocannabinoid activity in experimental models of acute and chronic pain, including inflammatory pain, neuropathic pain, and sickle cell disease. We also explore how these treatments alter nociceptive activity in the peripheral nervous system

Cisplatin and the Mu Opioid Receptor Antagonist Methylnaltrexone Inhibit Neurite Growth in Cultured Trigeminal Neurons

https://openworks.mdanderson.org/sumexp23/1040/thumbnail.jp

ApoA-I binding protein (AIBP) decreases mechanical hypersensitivity after plantar incision in a rat model of post-operative pain

https://openworks.mdanderson.org/sumexp22/1090/thumbnail.jp

The anterior cingulate cortex and pain processing

The neural network that contributes to the suffering which accompanies persistent pain states involves a number of brain regions. Of primary interest is the contribution of the cingulate cortex in processing the affective component of pain. The purpose of this review is to summarize recent data obtained using novel behavioral paradigms in animals based on measuring escape and/or avoidance of a noxious stimulus. These paradigms have successfully been used to study the nature of the neuroanatomical and neurochemical contributions of the anterior cingulate cortex to higher order pain processing in rodents

FaDu Human Squamous Cell Carcinoma Induces Hyperexcitability of Primary Sensory Neurons

https://openworks.mdanderson.org/sumexp21/1219/thumbnail.jp