MC4 Receptor as a Potential Target for Treating Rats with Co-Morbid Pain Disorders
Location
Medical Education Building, LSUHSC-NO
Presentation Date
10-10-2019 10:00 AM
End Date
10-10-2019 12:00 PM
Description
Pain is highly co-morbid with PTSD and AUD, but strategies are not adequate for treating individuals living with two or more of these diagnoses, and the neurobiological mechanisms underlying these disorders are not well defined. The ultimate goal of work in the Gilpin lab is to improve Veteran health and quality of life by guiding therapeutic strategies that reduce pain in individuals with PTSD and/or AUD. This work uses animal models to test the neurobiological mechanisms of increased pain sensitivity in individuals that have endured traumatic stress, are dependent on alcohol, or are in a state of chronic pain. Rodent models were used to examine the role of brain melanocortin-4 receptor (MC4R) signaling in hyperalgesia/allodynia in rats with chronic inflammatory pain. The specific aim of this project was to evaluate the anti-nociceptive effects of MC4R antagonist (HS014) on CFA injected rats using behavioral pharmacology techniques such as Von Frey (VF), Hargreaves’ (HG), and Mechanical Conflict System (MCS) testing. Complete Freund’s Adjuvant was injected into the rat’s back left paw, inducing inflammation, followed by an intracranial injection of HS014. Paw withdrawal time was determined for the controls and injected mice using the VF and HG methods. Time spent crossing the spike field in MCS at varying spike heights was determined. Significance was seen between the saline and CFA groups (p=0.02), indicating that the CFA did influence more inflammation, therefore lowering the pain threshold. Statistical significance between paw withdrawal times of the vehicle and HS014 antagonist groups in the HG experiments was also seen (p=0.03), suggesting that HS014 works as an analgesic for the CFA injected mice.
Recommended Citation
White, Donnell, "MC4 Receptor as a Potential Target for Treating Rats with Co-Morbid Pain Disorders" (2019). Medical Student Research Poster Symposium. 45.
https://digitalscholar.lsuhsc.edu/sommrd/2019/posters/45
MC4 Receptor as a Potential Target for Treating Rats with Co-Morbid Pain Disorders
Medical Education Building, LSUHSC-NO
Pain is highly co-morbid with PTSD and AUD, but strategies are not adequate for treating individuals living with two or more of these diagnoses, and the neurobiological mechanisms underlying these disorders are not well defined. The ultimate goal of work in the Gilpin lab is to improve Veteran health and quality of life by guiding therapeutic strategies that reduce pain in individuals with PTSD and/or AUD. This work uses animal models to test the neurobiological mechanisms of increased pain sensitivity in individuals that have endured traumatic stress, are dependent on alcohol, or are in a state of chronic pain. Rodent models were used to examine the role of brain melanocortin-4 receptor (MC4R) signaling in hyperalgesia/allodynia in rats with chronic inflammatory pain. The specific aim of this project was to evaluate the anti-nociceptive effects of MC4R antagonist (HS014) on CFA injected rats using behavioral pharmacology techniques such as Von Frey (VF), Hargreaves’ (HG), and Mechanical Conflict System (MCS) testing. Complete Freund’s Adjuvant was injected into the rat’s back left paw, inducing inflammation, followed by an intracranial injection of HS014. Paw withdrawal time was determined for the controls and injected mice using the VF and HG methods. Time spent crossing the spike field in MCS at varying spike heights was determined. Significance was seen between the saline and CFA groups (p=0.02), indicating that the CFA did influence more inflammation, therefore lowering the pain threshold. Statistical significance between paw withdrawal times of the vehicle and HS014 antagonist groups in the HG experiments was also seen (p=0.03), suggesting that HS014 works as an analgesic for the CFA injected mice.
Comments
Mentor: Nicholas W. Gilpin, PhD (Associate Professor, Physiology)