Congratulations to Waylin Yu, graduate student in the Kash Lab, who is a recipient of a prestigious Neuroscience Trainee Professional Development Award! He also won a Inscopix Tech Award and was a Mitchell Max Award finalist at the NIH Pain Consortium Symposium!
The Neuroscience Trainee Professional Development Award (TPDA) is a year-long merit-based professional development award program. As a TPDA recipient, Waylin will receive complimentary registration to attend Neuroscience 2019, which will be held October 19–23 in Chicago, and a check to help defray the cost of his travel to the meeting. He also will make a poster presentation October 21 at Neuroscience 2019. As a Mitchell Max Award finalist he gave an oral and poster presentation that was streamed and archived for the NIH.
The title of the presentation that won him Neuroscience development award and the Inscopix Tech Award, and for which he was a Mitchell Max Award finalist at the NIH Pain Consortium Symposium is “Cell type specific midbrain and extended amygdala contributions to sex differences in pain and drug use.
Chronic pain and drug abuse are comorbid disorders that manifest with differing prevalence and severity in males and females. A mechanism that explains sex-specific pain and drug interactions has yet to be identified. Recent evidence from our lab suggests that dopaminergic neurons of the ventrolateral periaqueductal grey (vlPAGDA+) contribute to the anti-nociceptive effects of morphine and alcohol use. Following up on these studies, we found that activation of vlPAGDA+ terminals in a primary output region, the bed nucleus of the stria terminalis (BNST), relieves thermal and mechanical nociception in males but not females. This effect persists during pathological pain, with vlPAGDA+/BNST activation attenuating heightened pain sensitivity following treatment with the inflammatory agent Complete Freund’s Adjuvant (CFA). Downstream of vlPAGDA+ neurons, we examined a population of pain- and alcohol-sensitive corticotropin releasing factor (CRF) neurons in the BNST. Genetic deletion of CRF from the BNST reduces thermal and mechanical nociception and potentiates alcohol consumption in male and female mice. In vivo miniscope calcium imaging of BNSTCRF+ neurons further reveal robust and synchronized recruitment of these neurons during acute exposure to pain and alcohol in both sexes. Taken together, these findings support the notion that vlPAGDA+ and BNSTCRF+neurons differentially contribute to sex-specific interactions of pain and drug use. This knowledge will be informative for future approaches to treating chronic pain and drug abuse, as it identifies new morphine- and alcohol-sensitive mechanisms that are capable of attenuating pain in both a sex-dependent and -independent manner.