Involvement of spinal cord δ opiate receptors in the antinociception of gestation and its hormonal simulation

Dawson-Basoa, Mary E.; Gintzler, Alan R.

doi:10.1016/s0006-8993(97)00092-9

Cited by 68 publications

(43 citation statements)

References 27 publications

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“…At the spinal level, opioid changes in late pregnancy have been investigated more extensively and the results indicate that spinal-opioid mediation of pregnancy-mediated analgesia is specific to y and n systems [16,17]. Consistent with this pattern of opioid receptor involvement are data showing that elevated pain-response thresholds evident during pregnancy are associated with enhancement in the activity of endogenous ligands of the y (enkephalin) and n (dynorphin) receptors [33,37,74].…”

Section: Discussionmentioning

confidence: 96%

Placenta ingestion by rats enhances δ- and κ-opioid antinociception, but suppresses μ-opioid antinociception

DiPirro

Kristal

2004

Brain Research

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Ingestion of placenta or amniotic fluid produces a dramatic enhancement of centrally mediated opioid antinociception in the rat. The present experiments investigated the role of each opioid receptor type (A, y, n) in the antinociception-modulating effects of Placental Opioid-Enhancing Factor (POEF-presumably the active substance). Antinociception was measured on a 52 jC hotplate in adult, female rats after they ingested placenta or control substance (1.0 g) and after they received an intracerebroventricular injection of a y-specific ([D-Pen2,D-Pen5]enkephalin (DPDPE); 0, 30, 50, 62, or 70 nmol), A-specific ([D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO); 0, 0.21, 0.29, or 0.39 nmol), or n-specific (U-62066; spiradoline; 0, 100, 150, or 200 nmol) opioid receptor agonist. The results showed that ingestion of placenta potentiated y-and n-opioid antinociception, but attenuated A-opioid antinociception. This finding of POEF action as both opioid receptor-specific and complex provides an important basis for understanding the intrinsic pain-suppression mechanisms that are activated during parturition and modified by placentophagia, and important information for the possible use of POEF as an adjunct to opioids in pain management. D

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Section: Discussionmentioning

confidence: 96%

Placenta ingestion by rats enhances δ- and κ-opioid antinociception, but suppresses μ-opioid antinociception

DiPirro

Kristal

2004

Brain Research

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“…In addition to antinociception, a slowed gut transit is characteristic of late pregnancy [4]. Of particular importance, here, are the findings that pregnancy antinociception is mediated by n-opioid [26] and y-opioid [5] receptors, that the opioid-based slowing of gut transit is mediated by A-opioid receptors [2,12,23,24,28], and that ingested placenta enhances n-and yreceptor-mediated antinociception but inhibits A-receptormediated antinociception [7]. Therefore, as suggested by the present results, ingestion of placenta or amniotic fluid at parturition may enhance the antinociception of pregnancy as well as help restore normal gut transit after parturition, particularly when transit has been slowed by activity at Aopioid receptors in the CNS.…”

Section: Discussionmentioning

confidence: 99%

Ingested placenta blocks the effect of morphine on gut transit in Long–Evans rats

Corpening¹,

Doerr²,

Kristal³

2004

Brain Research

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Opioids produce antinociception, and ingested placenta or amniotic fluid modifies that antinociception. More specifically, ingested placenta enhances the antinociception produced by selective activation of central n-opioid or y-opioid receptors but attenuates that produced by activation of central A-opioid receptors. Opioids also slow gut transit by acting on central or peripheral A-opioid receptors. Therefore, we hypothesized that ingested placenta would reverse the slowing of gut transit that is produced by morphine, a preferential A-opioid-receptor agonist. Rats were injected with morphine either centrally or systemically and fed placenta, after which gastrointestinal transit was evaluated. We report here that ingested placenta reversed the slowing of gut transit produced by centrally administered morphine but did not affect the slowing of gut transit produced by systemically administered morphine. These results suggest another likely consequence of placentophagia at parturition in mammals-reversal of opioid-mediated, pregnancy-based disruption of gastrointestinal function-as well as an important consideration in opioid-based treatments for pain in humans-enhancement of desirable effects with attenuation of adverse effects. D 2004 Elsevier B.V. All rights reserved.Theme: Endocrine and autonomic regulation Topic: Gastrointestinal and urogenital regulation

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“…Analgesia during pregnancy, or its hormonal simulation, is opioid-dependent in the rat as shown by the finding that it is abolished by the opiate antagonist naloxone Gintzler, 1980). It has been shown that this antinociception is mediated, at least to a large extent, by the activation of multiple spinal opioid systems involving -and -opioid receptors (Dawson-Basoa and Gintzler, 1997;Dawson-Basoa and Gintzler, 1998) even though peripheral as well as supraspinal mechanisms also contribute (Liu and Gintzler, 1999). Spinal dynorphin activity is central to the induction of pregnancy-induced analgesia and spinal dynorphin release is increased at least two-fold during hormone-simulated pregnancy (Gupta et al, 2001).…”

Section: Estrogen Receptor Neurons and The Endogenous Opioid Systemmentioning

confidence: 99%

Estrogenic influences in pain processing

Amandusson

Blomqvist

2013

Frontiers in Neuroendocrinology

109

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Gonadal hormones not only play a pivotal role in reproductive behavior and sexual differentiation, they also contribute to thermoregulation, feeding, memory, neuronal survival, and the perception of somatosensory stimuli. Numerous studies on both animals and human subjects have also demonstrated the potential effects of gonadal hormones, such as estrogens, on pain transmission. These effects most likely involve multiple neuroanatomical circuits as well as diverse neurochemical systems and they therefore need to be evaluated specifically to determine the localization and intrinsic characteristics of the neurons engaged. The aim of this review is to summarize the morphological as well as biochemical evidence in support for gonadal hormone modulation of nociceptive processing, with particular focus on estrogens and spinal cord mechanisms.

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Involvement of spinal cord δ opiate receptors in the antinociception of gestation and its hormonal simulation

Cited by 68 publications

References 27 publications

Placenta ingestion by rats enhances δ- and κ-opioid antinociception, but suppresses μ-opioid antinociception

Placenta ingestion by rats enhances δ- and κ-opioid antinociception, but suppresses μ-opioid antinociception

Ingested placenta blocks the effect of morphine on gut transit in Long–Evans rats

Estrogenic influences in pain processing

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