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Chronic pain debilitates millions of people worldwide, affecting an estimated 20% of adults. Unlike acute pain, chronic pain does not serve a protective purpose and instead debilitates patients. As responses to the opioid epidemic restrict opioid access, the need for non-addictive alternatives to opioid analgesics to treat chronic pain is rapidly growing. However, we do not yet fully understand how emotionally-inert sensory information is processed into the negative, unpleasant component of experiencing pain. Understanding this negative affective component of pain is the central goal of the Corder lab, with the eventual goal of identifying a translational target for novel, non-addictive analgesics. 

Through PURM, I had the opportunity to contribute to mapping pain’s affective pathway this summer. Dr. Corder’s previous work identified a critical network of neurons in the basolateral amygdala (BLA), an emotional processing center in the brain, as a nociceptive-responsive ensemble that is responsible for the negative affective component of pain processing. From there, we hypothesize these negative affective pain signals project to the anterior cingulate cortex (ACC), a region implicated in pain, emotion, and cognition. In addition to contributing to ongoing experiments, I had the opportunity to conduct a project of my own: mapping neural outputs from the ACC to further understand the brain regions responsible for the affective component of pain. 

Mapping the ACC’s outputs was a culmination of almost all of the techniques I learned this summer. These techniques included stereotaxic mouse brain surgeries, injections, perfusions, thinly slicing brain tissue, mounting tissue slices onto slides, immunohistochemistry, and microscope imaging. In essence, I used a combination of viruses to fluorescently label ACC neurons and their outputs that were activated by a painful stimulus. After enhancing the fluorescent signal with immunohistochemistry, my microscope images showed the neurons that were activated by pain in the ACC. This confirmed that nociceptive ACC neurons could be genetically accessed with the new viral technique. The viral techniques will allow further investigation into the ACC’s function, in conjunction with opto- and chemo-genetic tools to manipulate the ACC’s activity. 

As my first extended research experience, this summer served not only as my introduction to neuroscience concepts and techniques but also to the larger process of scientific inquiry. With little background in neuroscience, I read reviews and primary literature and asked questions, big and small, to get up to speed. Once situated, I also gained experience framing a research question and hypothesis, analyzing data, troubleshooting unexpected situations, and presenting research findings. Thanks to this summer, I am excited to explore how engineering and neuroscience connect and for future research experiences to come.

Chronic pain debilitates millions of people worldwide, affecting an estimated 20% of adults. Unlike acute pain, chronic pain does not serve a protective purpose and instead debilitates patients. As responses to the opioid epidemic restrict opioid access, the need for non-addictive alternatives to opioid analgesics to treat chronic pain is rapidly growing. However, we do not yet fully understand how emotionally-inert sensory information is processed into the negative, unpleasant component of experiencing pain. Understanding this negative affective component of pain is the central goal of the Corder lab, with the eventual goal of identifying a translational target for novel, non-addictive analgesics. 

Through PURM, I had the opportunity to contribute to mapping pain’s affective pathway this summer. Dr. Corder’s previous work identified a critical network of neurons in the basolateral amygdala (BLA), an emotional processing center in the brain, as a nociceptive-responsive ensemble that is responsible for the negative affective component of pain processing. From there, we hypothesize these negative affective pain signals project to the anterior cingulate cortex (ACC), a region implicated in pain, emotion, and cognition. In addition to contributing to ongoing experiments, I had the opportunity to conduct a project of my own: mapping neural outputs from the ACC to further understand the brain regions responsible for the affective component of pain. 

Mapping the ACC’s outputs was a culmination of almost all of the techniques I learned this summer. These techniques included stereotaxic mouse brain surgeries, injections, perfusions, thinly slicing brain tissue, mounting tissue slices onto slides, immunohistochemistry, and microscope imaging. In essence, I used a combination of viruses to fluorescently label ACC neurons and their outputs that were activated by a painful stimulus. After enhancing the fluorescent signal with immunohistochemistry, my microscope images showed the neurons that were activated by pain in the ACC. This confirmed that nociceptive ACC neurons could be genetically accessed with the new viral technique. The viral techniques will allow further investigation into the ACC’s function, in conjunction with opto- and chemo-genetic tools to manipulate the ACC’s activity. 

As my first extended research experience, this summer served not only as my introduction to neuroscience concepts and techniques but also to the larger process of scientific inquiry. With little background in neuroscience, I read reviews and primary literature and asked questions, big and small, to get up to speed. Once situated, I also gained experience framing a research question and hypothesis, analyzing data, troubleshooting unexpected situations, and presenting research findings. Thanks to this summer, I am excited to explore how engineering and neuroscience connect and for future research experiences to come.