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NIH Budget Stalls

NIH Budget Stalls Pain in the Brain A common variation in a gene coding for a key brain enzyme increases susceptibility to pain, report researchers from the University of Michigan Medical Center and the National Institute on Alcoholism and Alcohol Abuse (NIAAA). The enzyme, catechol O-methyltransferase (COMT), is vital to normal brain function, as it metabolizes the neurotransmitters norepinephrine and dopamine. The genetic variation changes a valine amino acid to a methionine, resulting in a three- to four-fold reduction in COMT's efficiency. Such a reduction leads to chronic overactivation of dopamine circuits, which in turn reduces activation of pain-relieving µ-opioid receptors, said David Goldman, MD, chief of the laboratory of neurogenetics at NIAAA. Goldman and colleagues found support for that conclusion by subjecting volunteers to a "pain challenge" while monitoring them with positron emission tomography (PET). The researchers also used questionnaires to measure emotional responses to pain in the 15 men and 14 women enrolled in the study. During the PET scans, a radioactive tracer that binds to µ-opioid receptors indicated each volunteer's response to an infusion of painful (hypertonic) or nonpainful (isotonic) saline solutions. As expected, volunteers with the lowest COMT activity displayed the lowest level of µ-opioid activation and reported more painful subjective experiences. Volunteers with the highest COMT activity exhibited the opposite effects. The differences in µ-opioid activation were most prominent in the thalamus, a sensory relay station, and the amygdala, an emotional center. About 16% of the population carries the genetic variation corresponding to low COMT activity and heightened pain response (Science. 2003;299:1240-1244). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA American Medical Association

NIH Budget Stalls

Vastag, Brian
JAMA , Volume 289 (11) – Mar 19, 2003
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NIH Budget Stalls

Abstract

Pain in the Brain A common variation in a gene coding for a key brain enzyme increases susceptibility to pain, report researchers from the University of Michigan Medical Center and the National Institute on Alcoholism and Alcohol Abuse (NIAAA). The enzyme, catechol O-methyltransferase (COMT), is vital to normal brain function, as it metabolizes the neurotransmitters norepinephrine and dopamine. The genetic variation changes a valine amino acid to a methionine, resulting in a three- to...
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Publisher
American Medical Association
Copyright
Copyright © 2003 American Medical Association. All Rights Reserved.
ISSN
0098-7484
eISSN
1538-3598
DOI
10.1001/jama.289.11.1368-a
Publisher site
See Article on Publisher Site

Abstract

Pain in the Brain A common variation in a gene coding for a key brain enzyme increases susceptibility to pain, report researchers from the University of Michigan Medical Center and the National Institute on Alcoholism and Alcohol Abuse (NIAAA). The enzyme, catechol O-methyltransferase (COMT), is vital to normal brain function, as it metabolizes the neurotransmitters norepinephrine and dopamine. The genetic variation changes a valine amino acid to a methionine, resulting in a three- to four-fold reduction in COMT's efficiency. Such a reduction leads to chronic overactivation of dopamine circuits, which in turn reduces activation of pain-relieving µ-opioid receptors, said David Goldman, MD, chief of the laboratory of neurogenetics at NIAAA. Goldman and colleagues found support for that conclusion by subjecting volunteers to a "pain challenge" while monitoring them with positron emission tomography (PET). The researchers also used questionnaires to measure emotional responses to pain in the 15 men and 14 women enrolled in the study. During the PET scans, a radioactive tracer that binds to µ-opioid receptors indicated each volunteer's response to an infusion of painful (hypertonic) or nonpainful (isotonic) saline solutions. As expected, volunteers with the lowest COMT activity displayed the lowest level of µ-opioid activation and reported more painful subjective experiences. Volunteers with the highest COMT activity exhibited the opposite effects. The differences in µ-opioid activation were most prominent in the thalamus, a sensory relay station, and the amygdala, an emotional center. About 16% of the population carries the genetic variation corresponding to low COMT activity and heightened pain response (Science. 2003;299:1240-1244).

Journal

JAMA – American Medical Association

Published: Mar 19, 2003

Keywords: pain,brain

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