Biography:

In the past Gayle G. Page has collaborated on articles with Przemyslaw Marek and Robert R. Edwards. One of their most recent publications is N-methyl-d-aspartic acid (NMDA) receptor antagonist MK-801 blocks non-opioid stress-induced analgesia. I. Comparison of opiate receptor-deficient and opiate receptor-rich strains of mice. Which was published in journal Brain Research.

More information about Gayle G. Page research including statistics on their citations can be found on their Copernicus Academic profile page.

Gayle G. Page's Articles: (4)

N-methyl-d-aspartic acid (NMDA) receptor antagonist MK-801 blocks non-opioid stress-induced analgesia. I. Comparison of opiate receptor-deficient and opiate receptor-rich strains of mice

AbstractThe effects of the specific N-methyl-d-aspartic acid (NMDA) receptor antagonist MK-801 (0.075 mg/kg), and the specific opiate receptor antagonist naloxone (10 mg/kg), on swim stress-induced analgesia (SSIA) were studied in opiate receptor-deficient (CXBK) and opiate receptor-rich (CXBH) mice. Animals were subjected to forced swimming, and analgesia was assessed using the hot-plate test. In CXBK mice SSIA was blocked by MK-801 but was completely insensitive to naloxone. In CXBH mice SSIA was partially attenuated both by naloxone and MK-801, and it was nearly abolished by a combination of these drugs. Morphine analgesia (10 mg/kg) was abolished by naloxone but completely unaffected by MK-801 in CXBH mice. These findings suggest that the NMDA receptor is critically involved in the non-opioid component of SSIA.

Association of catastrophizing with interleukin-6 responses to acute pain

AbstractCatastrophizing exerts its deleterious effects on pain via multiple pathways, and some researchers have reported that high levels of catastrophizing are associated with enhanced physiological reactivity to painful stimulation. In this project, 42 generally healthy adults underwent a series of psychophysical pain testing procedures assessing responses to noxious mechanical, heat, and cold stimuli. Pain catastrophizing cognitions were assessed prior to and then immediately after the various pain induction procedures. Blood samples were taken at baseline and then at several time points from the end of the procedures to 1 h post-testing. Samples were assayed for serum levels of cortisol and interleukin-6 (IL-6). Both cortisol and IL-6 increased from baseline during the post-testing period (p’s < .05), with cortisol returning to baseline by 1 h post-testing and IL-6 remaining elevated. Pain catastrophizing, measured immediately after the pain procedures, was unrelated to cortisol reactivity, but was strongly related to IL-6 reactivity (p < .01), with higher levels of catastrophizing predicting greater IL-6 reactivity. In multivariate analyses, the relationship between catastrophizing and IL-6 reactivity was independent of pain ratings. Collectively, these findings suggest that cognitive and emotional responses during the experience of pain can shape pro-inflammatory immune system responses to noxious stimulation. This pathway may represent one important mechanism by which catastrophizing and other psychosocial factors shape the experience of both acute and chronic pain in a variety of settings.

Proceedings of the Symposium “Updates of the Clinical Pharmacology of Opioids with Special Attention to Long-Acting Drugs”Immunologic Effects of Opioids in the Presence or Absence of Pain

AbstractOpioids are acknowledged to suppress immune functions following both acute and chronic administration; however, there appear to be differences according to the schedule of administration as well as the state of the organism. For example, whereas a single dose of morphine in the absence of pain is well known to be immune suppressive, the biologic consequences of this suppression are largely unknown. Repeated and chronic opioid ingestion in the absence of pain appears to result in significant consequences including high infectious disease prevalence. On the other hand, in the presence of acute pain, there is evidence that opioid administration in analgesic doses is protective. Much less is known regarding the immune and disease implications related to chronic opioid treatment for chronic pain states.

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