Behavioral Basis of Pain & Itch
How does our nervous system sense, perceive, and respond to stimuli causing pain and itch? We use genetic and behavioral techniques in mice to uncover the underlying molecules, cells, and circuits.
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Major Questions
How does our brain direct defensive responses to noxious stimuli?
How does our brain direct defensive responses to noxious stimuli?
Stepping barefoot on a pin could be excruciatingly painful and would evoke both a rapid physical reaction and an emotional response. We may rub our feet where it hurts, scream in pain, and move away from the spot to avoid re-stepping on the pin to avoid experiencing the pain a second time. We would also remember the spot on the floor where the pin was and avoid the area until we knew no more pins were lying around. A relatively inconsequential event could momentarily take over our physical and mental faculties and produce long-lasting behavioral changes. In our laboratory, we seek to understand how specific groups of neurons in the brain can drive specific aspects of such defensive behaviors. How do these neurons receive the pain information? What are their molecular characteristics? What is their anatomical architecture? How do these neurons communicate with the rest of the nervous system? We intend to answer these questions by leveraging molecular and optogenetic tools to manipulate behavior, map circuits, and record neural activity in mice.
Stepping barefoot on a pin could be excruciatingly painful and would evoke both a rapid physical reaction and an emotional response. We may rub our feet where it hurts, scream in pain, and move away from the spot to avoid re-stepping on the pin to avoid experiencing the pain a second time. We would also remember the spot on the floor where the pin was and avoid the area until we knew no more pins were lying around. A relatively inconsequential event could momentarily take over our physical and mental faculties and produce long-lasting behavioral changes. In our laboratory, we seek to understand how specific groups of neurons in the brain can drive specific aspects of such defensive behaviors. How do these neurons receive the pain information? What are their molecular characteristics? What is their anatomical architecture? How do these neurons communicate with the rest of the nervous system? We intend to answer these questions by leveraging molecular and optogenetic tools to manipulate behavior, map circuits, and record neural activity in mice.
Here, we have used optogenetic, chemogenetic, and anatomical viral mapping tools to reveal a trisynaptic neural pathway that mediated stress-induced analgesia in mice.
What are the maladaptive mechanisms underlying chronic pain and itch?
Pain and itch are fundamentally protective. However, these useful protective mechanisms can become a burden when they become chronic or outlast the stimulus. When and where these otherwise beneficial mechanisms become pathological remains poorly understood. Our laboratory studies how these conditions might be linked to alterations in specific brain areas regarding their connectivity, molecular composition, and activity.
Pain and itch are fundamentally protective. However, these useful protective mechanisms can become a burden when they become chronic or outlast the stimulus. When and where these otherwise beneficial mechanisms become pathological remains poorly understood. Our laboratory studies how these conditions might be linked to alterations in specific brain areas regarding their connectivity, molecular composition, and activity.
How do neuropeptides and neuromodulators drive plasticity in pain and itch circuits?
How do neuropeptides and neuromodulators drive plasticity in pain and itch circuits?
The neural circuits for pain and itch are incredibly plastic. Repeated exposure to the stimuli causing pain and itch can alter the activity in these circuits for the long term. These long-term changes often result in pathological chronic pain and itch. Neuropeptides and neuromodulators released by the neurons in these circuits are the major players that bring about neural plasticity. In our laboratory, we use recently developed in-vivo fluorescent sensors for specific neuromodulators and peptides, such as serotonin, dopamine, nor-epinephrine, and substance P, among others, to determine how the dynamics of these molecules change in the circuits for chronic pain and itch.
The neural circuits for pain and itch are incredibly plastic. Repeated exposure to the stimuli causing pain and itch can alter the activity in these circuits for the long term. These long-term changes often result in pathological chronic pain and itch. Neuropeptides and neuromodulators released by the neurons in these circuits are the major players that bring about neural plasticity. In our laboratory, we use recently developed in-vivo fluorescent sensors for specific neuromodulators and peptides, such as serotonin, dopamine, nor-epinephrine, and substance P, among others, to determine how the dynamics of these molecules change in the circuits for chronic pain and itch.
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