Category
Poster - Basic
Description
Neuropathic pain is a chronic pathology of the nervous system (Finnerup et al., 2021), often related to inflammatory conditions, including multiple sclerosis (MS) and Guillain-Barre syndrome (GBS) (Ubogu, 2015). In vitro and vivo studies have investigated the role of proinflammatory cytokines, chemokines, and other inflammatory mediators within the spinal cord (SC) for the development and persistence of neuropathic pain (Tsuda, 2017; Gwak, 2012). In vivo studies have established a formalin-induced pain model in rats to be comparable to spinal nerve ligation (SNL) and induce persistent spinal inflammation (Salinas-Abarca, 2017). It remains unknown whether a formalin-induced pain model can induce neuropathic pain in mice. Our research aims to investigate whether a formalin-induced pain model can induce persistent neuropathic inflammatory pain in mice and to study consequent in vivo mechanisms. Our research will modify this existing protocol in C57BL/6 mice; following formalin injection, mice will be assessed for pain sensitivity over a two-week period and sacrificed to collect whole SC’s for the following: 1) flow cytometry to detect immune cell infiltration; 2) histological observations using Luxol Fast Blue (LFB) and Golgi stains for qualitative analysis of myelin and neuron morphology and distribution; 3) immunohistochemical markers for glia activation and neuronal pathology, such as Glial Fibrillary Acidic Protein (GFAP) and Ionized Calcium Adaptor Protein 1 (Iba1) and Neuronal Nuclear protein (NeuN). Determining the efficacy of formalin-induced pain models in mice provides potential in other animal models including experimental autoimmune encephalomyelitis (EAE), which simulate MS as an inflammatory demyelinating disease (Gold, 2006). Our research investigates the efficacy of a formalin-induced pain model to induce neuropathic pain in mice and studies the consequent molecular mechanisms to develop novel targeted therapeutics for inflammatory neuropathic pain condition.
Formalin-induced neuropathic pain in mice
Poster - Basic
Neuropathic pain is a chronic pathology of the nervous system (Finnerup et al., 2021), often related to inflammatory conditions, including multiple sclerosis (MS) and Guillain-Barre syndrome (GBS) (Ubogu, 2015). In vitro and vivo studies have investigated the role of proinflammatory cytokines, chemokines, and other inflammatory mediators within the spinal cord (SC) for the development and persistence of neuropathic pain (Tsuda, 2017; Gwak, 2012). In vivo studies have established a formalin-induced pain model in rats to be comparable to spinal nerve ligation (SNL) and induce persistent spinal inflammation (Salinas-Abarca, 2017). It remains unknown whether a formalin-induced pain model can induce neuropathic pain in mice. Our research aims to investigate whether a formalin-induced pain model can induce persistent neuropathic inflammatory pain in mice and to study consequent in vivo mechanisms. Our research will modify this existing protocol in C57BL/6 mice; following formalin injection, mice will be assessed for pain sensitivity over a two-week period and sacrificed to collect whole SC’s for the following: 1) flow cytometry to detect immune cell infiltration; 2) histological observations using Luxol Fast Blue (LFB) and Golgi stains for qualitative analysis of myelin and neuron morphology and distribution; 3) immunohistochemical markers for glia activation and neuronal pathology, such as Glial Fibrillary Acidic Protein (GFAP) and Ionized Calcium Adaptor Protein 1 (Iba1) and Neuronal Nuclear protein (NeuN). Determining the efficacy of formalin-induced pain models in mice provides potential in other animal models including experimental autoimmune encephalomyelitis (EAE), which simulate MS as an inflammatory demyelinating disease (Gold, 2006). Our research investigates the efficacy of a formalin-induced pain model to induce neuropathic pain in mice and studies the consequent molecular mechanisms to develop novel targeted therapeutics for inflammatory neuropathic pain condition.
Comments
Undergraduate