The Journal of neuroscience : the official journal of the Society for Neuroscience
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Professional neuroscience organizations have recently pledged their commitments to diversity, equity, and inclusion in examining institutional discrimination; to raise questions about how to train underrepresented scientists; and to recruit underrepresented subjects for a more equitable scientific enterprise in the 21st century. Studies have illuminated racial disparities in funding, likely because of implicit bias in the review process and differential access to resources. We propose that one concrete way to monitor and redress these disparities is to collect and publicize data on grantees by gender, race, ethnicity, and location from neuroscience funding agencies. Beyond remedying historical disadvantages, disseminating funding more equitably across recipients would be an empirical solution that can improve the very quality of neuroscience.
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As one of the thalamic midline nuclei, the thalamic paraventricular nucleus (PVT) is considered to be an important signal integration site for many descending and ascending pathways that modulate a variety of behaviors, including feeding, emotions, and drug-seeking. A recent study has demonstrated that the PVT is implicated in the acute visceral pain response, but it is unclear whether the PVT plays a critical role in the central processing of chronic pain. Here, we report that the neurons in the posterior portion of the PVT (pPVT) and their downstream pathway are involved in descending nociceptive facilitation regarding the development of neuropathic pain conditions in male rats. ⋯ Here, an integrative approach of behavioral tests, electrophysiology, and immunohistochemistry was used to advance the novel concept that the pPVT-CeA pathway activation facilitates neuropathic pain processing. Using rabies virus (RV)-based and cell-type-specific retrograde transsynaptic tracing techniques, we found that glutamatergic neurons in the vlPAG were the target of the pPVT-CeA pathway. Thus, this study indicates the involvement of a pPVTGlu+-CeA-vlPAGGlu+ pathway in a descending facilitatory mechanism underlying neuropathic pain.