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Stuart, B. A.

Publications and source records attributed to Stuart, B. A..

2 recordsLinked to original sources

Effects of gabapentin on ongoing behaviors displayed by mice with chemotherapy neuropathy

Chemotherapy-induced peripheral neuropathy (CIPN) is a common and painful side effect of paclitaxel (PTX) treatment. The most common measures of painful neuropathy focus on evoked mechanical hypersensitivity, but clinically relevant ongoing pain remains understudied in preclinical models. Automated machine learning methods for pose estimation and behavioral classification have been proposed to capture non-evoked pain-like behaviors, though these approaches have primarily been applied to unilateral injury models such as spared nerve injury or unilateral inflammatory compound injection. Here, we evaluated the extent to which paclitaxel-induced CIPN affects the posture and spontaneous behavior of freely moving mice using a commercially available automated recording system (BlackBox). We found that paclitaxel-treated mice develop a broad and reproducible behavioral and postural phenotype relative to vehicle-treated controls, characterized by reduced front paw luminance and print size, increased front paw lifting, and altered body measurements consistent with a guarded posture. This phenotype was replicated across two independent cohorts and was detectable at both day 2 and day 6 following the final paclitaxel injection. To identify behavioral features specific to CIPN, we administered gabapentin, an analgesic often used to treat neuropathic pain in patients, to determine whether paclitaxel-induced behavioral changes could be attenuated. Gabapentin reduced several behavioral features in both paclitaxel-treated and vehicle-treated animals, suggesting that its effects on posture and gait are not specific pain in CIPN. These findings demonstrate that automated behavioral recording captures a robust paclitaxel-induced postural phenotype but question whether captured behaviors are indicative of ongoing pain as alleviated by gabapentin.

neuroscience↗

Keratinocyte Pannexin-1 is essential for Mechanical Hypersensitivity following Traumatic Peripheral Nerve Injury

Neuropathic pain remains one of the most prevalent and challenging forms of chronic pain to manage. It is characterized by severe cutaneous touch and cold evoked pain. Whereas the contribution of peripheral nerves to neuropathic pain is well established, the influence of peripheral non-neuronal cells that interact with injured nerves has not been studied in depth. Keratinocytes, the primary cell type in the epidermis, play an important role in the initial processing of environmental mechanical and thermal stimuli under normal conditions. Here, we investigated the role of keratinocytes following traumatic peripheral nerve injury and determined that these cells contribute to injury-associated heightened sensation. We performed tibial spared nerve injury (tSNI) in mice that selectively express archaerhodopsin in keratinocytes to temporally reduce activity from these cells at various timepoints following injury. Brief (5 min) optogenetic inhibition completely reversed both the mechanical and cold hypersensitivity at acute (4 days) and throughout chronic (17 weeks) timepoints following tSNI. Keratinocytes isolated from the spared glabrous skin dermatome were sensitized to mechanical and cold stimuli and found to release factors that enhance activity of sensory neurons. Moreover, we found that keratinocyte phospholipase A2 (PLA2) driven activation of pannexin-1 is critical for the long term development of mechanical allodynia. This discovery indicates that keratinocytes contribute substantially to the mechanical and cold allodynia after traumatic nerve injury and suggest that keratinocytes may be a topical therapeutic target to alleviate the severe touch- and cold-evoked cutaneous pain following peripheral nerve injury.

neuroscience↗