| Literature DB >> 30878290 |
Nicolas Massaly1, Bryan A Copits1, Adrianne R Wilson-Poe1, Lucia Hipólito2, Tamara Markovic1, Hye Jean Yoon1, Shiwei Liu3, Marie C Walicki4, Dionnet L Bhatti1, Sunil Sirohi5, Amanda Klaas6, Brendan M Walker5, Rachael Neve7, Catherine M Cahill3, Kooresh I Shoghi8, Robert W Gereau9, Jordan G McCall4, Ream Al-Hasani10, Michael R Bruchas11, Jose A Morón12.
Abstract
Negative affective states affect quality of life for patients suffering from pain. These maladaptive emotional states can lead to involuntary opioid overdose and many neuropsychiatric comorbidities. Uncovering the mechanisms responsible for pain-induced negative affect is critical in addressing these comorbid outcomes. The nucleus accumbens (NAc) shell, which integrates the aversive and rewarding valence of stimuli, exhibits plastic adaptations in the presence of pain. In discrete regions of the NAc, activation of the kappa opioid receptor (KOR) decreases the reinforcing properties of rewards and induces aversive behaviors. Using complementary techniques, we report that in vivo recruitment of NAc shell dynorphin neurons, acting through KOR, is necessary and sufficient to drive pain-induced negative affect. Taken together, our results provide evidence that pain-induced adaptations in the kappa opioid system within the NAc shell represent a functional target for therapeutic intervention that could circumvent pain-induced affective disorders. VIDEO ABSTRACT.Entities:
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Year: 2019 PMID： 30878290 PMCID： PMC6509001 DOI： 10.1016/j.neuron.2019.02.029
Source DB: PubMed Journal: Neuron ISSN： 0896-6273 Impact factor: 17.173