Chronic exposure to morphine attenuates expression of interleukin-1β in the rat hippocampus

Patel, Nilesh A.; Romero, Alejandro A.; Zadina, James E.; Chang, Sulie L.

doi:10.1016/0006-8993(95)01575-2

Cited by 21 publications

(8 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This pattern of changes is the first of their kind reported. In contrast to our findings of both proinflammation and attenuation proinflammation in the hippocampus, Patel et al (1996) reported decreased IL-1β throughout hippocampus, using a much higher morphine regimen.…”

Section: Discussioncontrasting

confidence: 99%

Reduction of opioid withdrawal and potentiation of acute opioid analgesia by systemic AV411 (ibudilast)

Hutchinson¹,

Lewis²,

Coats³

et al. 2009

Brain, Behavior, and Immunity

227

210

View full text Add to dashboard Cite

Morphine-induced glial proinflammatory responses have been documented to contribute to tolerance to opioid analgesia. Here, we examined whether drugs previously shown to suppress glial proinflammatory responses can alter other clinically relevant opioid effects; namely, withdrawal or acute analgesia. AV411 (ibudilast) and minocycline, drugs with distinct mechanisms of action that result in attenuation of glial proinflammatory responses, each reduced naloxone-precipitated withdrawal. Analysis of brain nuclei associated with opioid withdrawal revealed that morphine altered expression of glial activation markers, cytokines, chemokines, and a neurotrophic factor. AV411 attenuated many of these morphine-induced effects. AV411 also protected against spontaneous withdrawal-induced hyperactivity and weight loss recorded across a 12-day timecourse. Notably, in the spontaneous withdrawal study, AV411 treatment was delayed relative to the start of the morphine regimen so to also test whether AV411 could still be effective in the face of established morphine dependence, which it was. AV411 did not simply attenuate all opioid effects, as co-administering AV411 with morphine or oxycodone caused 3-to-5-fold increases in acute analgesic potency, as revealed by leftward shifts in the analgesic dose response curves. Timecourse analyses revealed that plasma morphine levels were not altered by AV411, suggestive that potentiated analgesia was not simply due to prolongation of morphine exposure or increased plasma concentrations. These data support and extend similar potentiation of acute opioid analgesia by minocycline, again providing converging lines of evidence of glial involvement. Hence, suppression of glial proinflammatory responses can significantly reduce opioid withdrawal, whilst improving analgesia.

show abstract

Section: Discussioncontrasting

confidence: 99%

Reduction of opioid withdrawal and potentiation of acute opioid analgesia by systemic AV411 (ibudilast)

Hutchinson¹,

Lewis²,

Coats³

et al. 2009

Brain, Behavior, and Immunity

227

210

View full text Add to dashboard Cite

show abstract

“…Therefore, it is possible that chronic opiate and psychostimulant exposure alters growth factors in the hippocampus, which in turn inhibit SGZ proliferation. It is known that morphine inhibits hippocampal levels of the cytokine IL1b (Patel et al, 1996), and work from our laboratory shows a dynamic change in protein levels of many hippocampal growth factors, including BDNF, IGFI, IGFII, and IL1b, after chronic morphine in both rat and mouse . Current studies are examining when decreased proliferation occurs relative to changes in hippocampal growth factors during morphine exposure and withdrawal (Arguello et al, 2005).…”

Section: Proproliferative Environmentmentioning

confidence: 98%

Opiates, psychostimulants, and adult hippocampal neurogenesis: Insights for addiction and stem cell biology

2006

View full text Add to dashboard Cite

Once thought to produce global, nonspecific brain injury, drugs of abuse are now known to produce selective neuro-adaptations in particular brain regions. These neuro-adaptations are being closely examined for clues to the development, maintenance, and treatment of addiction. The hippocampus is an area of particular interest, as it is central to many aspects of the addictive process, including relapse to drug taking. A recently appreciated hippocampal neuro-adaptation produced by drugs as diverse as opiates and psychostimulants is decreased neurogenesis in the sub-granular zone (SGZ). While the role of adult-generated neurons is not clear, their functional integration into hippocampal circuitry raises the possibility that decreased adult SGZ neurogenesis may alter hippocampal function in such a way as to maintain addictive behavior or contribute to relapse. Here, we review the impact of opiates and psychostimulants on the different stages of cell development in the adult brain, as well as the different stages of the addictive process. We discuss how examination of drug-induced alterations of adult neurogenesis advances our understanding of the complex mechanisms by which opiates and psychostimulants affect brain function while also opening avenues for novel ways of assessing the functional role of adult-generated neurons. In addition, we highlight key discrepancies in the field and underscore the necessity to move "beyond BrdU"--beyond merely counting new hippocampal cells labeled with the S phase marker bromodeoxyuridine--so as to probe mechanistic questions about how drug-induced alterations in adult hippocampal neurogenesis occur and what the functional ramifications of alterations in neurogenesis are for addiction.

show abstract

“…It has been reported that prenatal morphine (GD12–GD18) suppressed the cytotoxic activity of NK cells and reduced LPS-induced fever in adult male rat offspring [34]. These results were probably a consequence of an immunomodulatory role of morphine on the cytokine network, including the release of known key molecules such as IL-1 and TNF-α [6, 29]. In vitro morphine treatment significantly enhanced HIV infection of neonatal monocyte-derived macrophages.…”

Section: Discussionmentioning

confidence: 88%

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Fonseca

Sakai²,

Carvalho-Freitas³

et al. 2005

Neuroendocrinology

View full text Add to dashboard Cite

The present study analyzed the effects of maternal stress (PS) and/or naloxone treatment on the activity of peritoneal macrophage in male and female Swiss mice offspring. Pregnant female rats received a daily footshock (0.2 mA) and/or a naloxone injection from gestational day 15 to 19. Experiments were performed on postnatal day 30 on male and female pups. The following results were obtained in male offspring: (1) PS decreased both the index and the percentage of phagocytosis, this decrement being reversed by naloxone treatment, and (2) naloxone alone decreased the percentage of phagocytosis. The following results were obtained in female offspring: (1) PS decreased spontaneous and phorbol myristate acetate-induced macrophage oxidative burst, this decrement being reversed by naloxone pretreatment, and (2) PS decreased both the index and percentage of the phagocytosis, this effect was prevented by naloxone treatment. These data are discussed focussing on a putative neuroimmune interaction involving opioidergic systems during the ontogeny of the central nervous and immune systems.

show abstract

Chronic exposure to morphine attenuates expression of interleukin-1β in the rat hippocampus

Cited by 21 publications

References 13 publications

Reduction of opioid withdrawal and potentiation of acute opioid analgesia by systemic AV411 (ibudilast)

Reduction of opioid withdrawal and potentiation of acute opioid analgesia by systemic AV411 (ibudilast)

Opiates, psychostimulants, and adult hippocampal neurogenesis: Insights for addiction and stem cell biology

Naloxone Treatment Prevents Prenatal Stress Effects on Peritoneal Macrophage Activity in Mice Offspring

Contact Info

Product

Resources

About