Tyr‐MIF‐1 attenuates antinociceptive responses induced by three models of stress‐analgesia

Galina, Zvi Harry; Kastin, Abba J.

doi:10.1111/j.1476-5381.1987.tb11219.x

Cited by 33 publications

(2 citation statements)

References 30 publications

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“…Consistent with its antiopiate actions, Tyr-MIF-1 has been shown to reduce stress-induced analgesia in mice [23] , The present findingsofTyr-MIF-l-LI in the adrenal medulla would seem to suggest an expanded role for the adrenals in stress-induced analgesia. It does not easily ex plain, however, the report of increased sensitivity to the hy pothermic effect of morphine and |5-endorphin in adrenalectomized mice [24].…”

Section: Discussionsupporting

confidence: 67%

Uptake, Content Regulation of Plasma Concentrations, and Binding of Tyr-MIF-1 by the Adrenals

Kastin¹,

Fabre²,

Banks³

et al. 1993

Neuroendocrinology

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The known occurrence of opiates in the adrenals stimulated us to determine whether Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH₂), an endogenous peptide that can act as an antiopiate, is present in these glands and whether adrenalectomy affects its concentrations in plasma. The presence of Tyr-MIF-1 in the adrenals of the rat was shown by radioimmunoassay (RIA) and high performance liquid chromatography (HPLC). Binding sites for the tetrapeptide also were found in the adrenal. The concentrations and binding of Tyr-MIF-1 were higher in the adrenal medulla than in the adrenal cortex. The adrenals preferentially trapped ¹²⁵I-Tyr-MIF-l as compared with ^99mTc-albumin after intravenous administration. However, after correction for tissue weight and vascular space, accumulation of ¹²⁵I-Tyr-MIF-1 by the adrenals was in the general range seen for several other tissues. The concentrations of Tyr-MIF-1-like immunoreactivity determined by RIA in the plasma of adrenalectomized rats were increased in comparison with sham operated or unoperated controls. This approximate doubling was unchanged by the site of sampling: hepatic portal vein, renal vein, inferior vena cava, jugular vein, or truncal blood. Hypophysectomy, removal of the adrenal medulla, or treatment with corticosterone also did not block this increase. Tyr-MIF-1-like immunoreactivity in the plasma of adrenalectomized rats eluted at the same position by HPLC as did the synthetic Tyr-MIF-1 standard. Thus, the adrenal gland contains Tyr-MIF-1 and can affect its concentrations in plasma.

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Section: Discussionsupporting

confidence: 67%

Uptake, Content Regulation of Plasma Concentrations, and Binding of Tyr-MIF-1 by the Adrenals

Kastin¹,

Fabre²,

Banks³

et al. 1993

Neuroendocrinology

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“…Thus this model allows for tolerance and dependence to be separable. Moreover, since the antiopioids probably have different neuroanatomical distri- (Kastin et al, 1984) (Galina and Kastin, 1987) Dynorphin (1-13) attenuates P-endorphin Dynorphin (1-13) exhibits mu-antagonist actions in (Friedman et al, 1981) (Holaday et al, 1986) antinociception endotoxemic shock, fluorthyl-induced seizures, and DADL-induced increases in striatal CAMP Spinal dynorphin (1-17) acts as a n anti-analgesic Dynorphin (1-17) attenuated morphine-and (Fujimoto and Arts, 1990;Fujimoto et al, 1990a,bJ (Sheldon et al, 1989 normorphin-induced contractions of the rat urinary bladder Dynorphin mediates in part the tolerance produced by a single large dose of morphine Dynorphin may oppose the rewarding effects of morphine Pfeiffer et al, 1986) (Fujimoto and Holmes, 1990;Sofuoglu and Takemori, (Di Chiara and Imperato, 1988a,b;Kurnor et al, 1986; (Dourish et al, 1990;Faris et al, 1983) (Dourish et al, 1990) (Itoh and Katsuura, 1981) (Bhargava et al, 1983;Holaday et al, 1978) (Bhargava et al, 1983;Holaday et al, 1978) (Bhargava et al, 1983) (Bhargava et al, 1983) dependence hypothermia and catalepsy morphine-induced antinociception @-endorphin (1-31) p-Endorphin (1-27) Antagonizes @-endorphin (1-33 J antinociception Nicolas et al, 1984) butions, the model clearly allows for tolerance and dependence to be anatomically separable. As pointed out by Smith et al (19881, a n anti-opioid model which postulates the existence of AOP which do not bind to opioid receptors, cannot explain the high degrees of tolerance which can be achieved.…”

Section: Introductionmentioning

confidence: 99%

A review of the role of anti‐opioid peptides in morphine tolerance and dependence

Rothman¹

1992

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155

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Studies on the mechanisms of tolerance and dependence have mostly focused on changes at the receptor level. These experiments, conducted with model systems ranging from clonal cell lines to whole animals, have identified a number of important adaptive mechanisms which occur at the receptor level. However, none of these adaptive mechanisms can completely account for the phenomena which serve to define the state of morphine tolerance and dependence, especially the observation that as an animal becomes more tolerant to morphine, less naloxone is required to trigger withdrawal. The data reviewed in this paper provide strong support for the hypothesis that the brain synthesizes and secretes neuropeptides which act as part of a homeostatic system to attenuate the effects of morphine and endogenous opioid peptides. According to this model, administration of morphine releases anti-opioid peptides (AOP), which then attenuate the effects of morphine. As more morphine is given, more AOP are released, thereby producing tolerance to the effects of morphine. Cessation of morphine administration, or administration of naloxone, produces a relative excess of anti-opioid, which is in part responsible for the withdrawal syndrome. Since endogenous and exogenous antagonists might together produce synergistic effects, less naloxone might be required to trigger withdrawal in the presence of higher levels of AOPs. Although the study of AOP is in its infancy, a deeper understanding of the central nervous system (CNS) anti-opioid systems may lead to new treatments for chronic pain, substance abuse, and psychiatric disorders.

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Social conflict-induced changes in nociception and β-endorphin-like immunoreactivity in pituitary and discrete brain areas of C57BL/6 and DBA/2 mice

et al. 1988

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Tyr‐MIF‐1 attenuates antinociceptive responses induced by three models of stress‐analgesia

Cited by 33 publications

References 30 publications

Uptake, Content Regulation of Plasma Concentrations, and Binding of Tyr-MIF-1 by the Adrenals

Uptake, Content Regulation of Plasma Concentrations, and Binding of Tyr-MIF-1 by the Adrenals

A review of the role of anti‐opioid peptides in morphine tolerance and dependence

Social conflict-induced changes in nociception and β-endorphin-like immunoreactivity in pituitary and discrete brain areas of C57BL/6 and DBA/2 mice

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