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Prominent interindividual and sex-dependent differences have been described in responses to sustained pain and other stressful stimuli. Variations in mu-opioid receptor-mediated endogenous opioid neurotransmission may underlie some of these processes. We examined both baseline mu-opioid receptor levels and the activation of this neurotransmitter system during sustained pain using positron emission tomography in a sample of young healthy men and women. Women were studied twice, during low and high estrogen states. The high-estrogen state was associated with regional increases in baseline mu-opioid receptor availability in vivo and a greater activation of endogenous opioid neurotransmission during the pain stressor. The latter did not differ from that obtained in males. During the low estrogen condition, however, significant reductions in endogenous opioid tone were observed at the level of thalamus, nucleus accumbens, and amygdala, which were associated with hyperalgesic responses. Estrogen-associated variations in the activity of mu-opioid neurotransmission correlated with individual ratings of the sensory and affective perceptions of the pain and the subsequent recall of that experience. These data demonstrate a significant role of estrogen in modulating endogenous opioid neurotransmission and associated psychophysical responses to a pain stressor in humans.

Original publication

DOI

10.1523/JNEUROSCI.5223-05.2006

Type

Journal article

Journal

The journal of neuroscience : the official journal of the society for neuroscience

Publication Date

05/2006

Volume

26

Pages

5777 - 5785

Addresses

Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan 48109, USA.

Keywords

Brain, Humans, Pain, Estradiol, Receptors, Opioid, mu, Analgesics, Narcotics, Sex Factors, Synaptic Transmission, Adult, Female, Male