Diminished neurokinin-1 receptor availability in patients with two forms of chronic visceral pain |
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| Authors: | Johanna M. Jarcho Natasha A. Feier Alberto Bert Jennifer A. Labus Maunoo Lee Jean Stains Bahar Ebrat Stephanie M. Groman Kirsten Tillisch Arthur L. Brody Edythe D. London Mark A. Mandelkern Emeran A. Mayer |
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| Affiliation: | 1. Section on Developmental and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, USA;2. Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA;3. Alan Edwards Centre for Research on Pain, Faculty of Dentistry, McGill University, Montreal, QC, Canada;4. im3D Medical Imaging Lab, S.p.A, Torino, Italy;5. Department of Psychology, UCLA, Los Angeles, CA, USA;6. Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA;g VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA;h Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA;i Department of Physics, University of California, Irvine, CA, USA |
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| Abstract: | Central sensitization and dysregulation of peripheral substance P and neurokinin-1 receptor (NK-1R) signaling are associated with chronic abdominal pain in inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Although positron emission tomography (PET) has demonstrated that patients with injury-related chronic pain have diminished NK-1R availability in the brain, it is unknown whether these deficits are present in IBD and IBS patients, who have etiologically distinct forms of non-injury-related chronic pain. This study’s aim was to determine if patients with IBD or IBS exhibit deficits in brain expression of NK-1Rs relative to healthy controls (HCs), the extent to which expression patterns differ across patient populations, and if these patterns differentially relate to clinical parameters. PET with [18F]SPA-RQ was used to measure NK-1R availability by quantifying binding potential (BP) in the 3 groups. Exploratory correlation analyses were performed to detect associations between NK-1R BP and physical symptoms. Compared to HCs, IBD patients had NK-1R BP deficits across a widespread network of cortical and subcortical regions. IBS patients had similar, but less pronounced deficits. BP in a subset of these regions was robustly related to discrete clinical parameters in each patient population. Widespread deficits in NK-1R BP occur in IBD and, to a lesser extent, IBS; however, discrete clinical parameters relate to NK-1R BP in each patient population. This suggests that potential pharmacological interventions that target NK-1R signaling may be most effective for treating distinct symptoms in IBD and IBS. |
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| Keywords: | PET NK-1 receptor Irritable bowel syndrome Inflammatory bowel disease Somatic pain Quality of life |
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