INT7833
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In this work we have shown, by in vivo binding experiments, that the endogenous enkephalins, protected from degrading enzymes by mixed inhibitors such as kelatorphan and N-[(R,S)-2-benzyl-3-[(S)-2-amino-4-methylthiobutyldithio]-1-oxo pro pyl]- L-phenylalanine benzyl ester (RB 101), a systemically active prodrug, modulate CCK release in mouse brain, leading to an overall increase in the extracellular levels of CCK. | |||||||||||||||
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RESULTS: In the plantar analgesia test the latency of hind paw withdrawal was significantly increased in CCK(2) receptor deficient mice compared to wild-type (+/+) littermates. | |||||||||||||||
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The antinociceptive activity of SNF9007 was not a result of the activation of CCK receptors, as treatment with either CCK-A or CCK-B receptor antagonist was ineffective in blocking SNF9007 antinociception. | |||||||||||||||
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Previous work indicates that the antianalgesic action of pentobarbital and neurotensin administered intracerebroventricularly in mice arises from activation of a descending system to release cholecystokinin (CCK) in the spinal cord where CCK is known to antagonize morphine analgesia. | |||||||||||||||
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Previous work indicates that the antianalgesic action of pentobarbital and neurotensin administered intracerebroventricularly in mice arises from activation of a descending system to release cholecystokinin (CCK) in the spinal cord where CCK is known to antagonize morphine analgesia. | |||||||||||||||
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In contrast, 3R[+]-N-[2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-benzodiazepin-3-yl ]-N'- [3-methyl-phenyl]urea (L365,260), a selective CCKB receptor antagonist, blocked the action of CCK4(30-33) and SNF 9007 (phase I), and also antagonized CCK8(s), though to a lesser degree. | |||||||||||||||
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These data demonstrate that the blockade of endogenous CCK actions leads to morphine sensitization probably through both CCK receptors. | |||||||||||||||
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Seizures induce dramatic and distinctly different changes in enkephalin, dynorphin, and CCK immunoreactivities in mouse hippocampal mossy fibers. | |||||||||||||||
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The stimulation of CCK(A) receptors seems to increase the release of endogenous enkephalins. | |||||||||||||||
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In these animals, which were tested for antinociception on the 5th day, tolerance to the drug (3, 6 and 9 mg/kg s.c.) was also decreased by caerulein, CCK-8 but not unsulfated CCK-8. | |||||||||||||||
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It is concluded that the cholecystokinin agonist caerulein potentiated the morphine response by stimulation of cholecystokinin-A and/or cholecystokinin-B receptors. | |||||||||||||||
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It is concluded that the cholecystokinin agonist caerulein potentiated the morphine response by stimulation of cholecystokinin-A and/or cholecystokinin-B receptors. | |||||||||||||||
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Gene expression analysis revealed an up-regulation of CCK(2) receptor gene in the lumbar spinal cord and mesolimbic area in wild-type mice in response to stress. | |||||||||||||||
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Cholecystokinin2 (CCK2) receptor-deficient mice were used to analyze the in vivo function of CCK2 receptor and especially the incidence of this gene invalidation on enkephalinergic and dopaminergic systems. | |||||||||||||||
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As in other experimental paradigms, CCK(A) and CCK(B) receptor stimulation appears to have opposite effects in modulating opioidergic activity. | |||||||||||||||
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As in other experimental paradigms, CCK(A) and CCK(B) receptor stimulation appears to have opposite effects in modulating opioidergic activity. | |||||||||||||||
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The existence of regulatory loops between both systems has been proposed, and the physiological antagonism between CCK, through activation of CCK2 receptors, and endogenous opioid systems has been demonstrated. | |||||||||||||||
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The results suggest that activation of CCK-A receptors by BDNL leads to antinociceptive responses indirectly mediated by stimulation of mu-opioid receptors by endogenous enkephalins. | |||||||||||||||
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These findings again suggest that the effect of CART peptide was pronounced through activation of CCK-A receptor and point to satiety-related sedation. | |||||||||||||||
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The action of CCK on CART expression was shown to be mediated by activation of protein kinase C and cAMP response element binding protein (CREB) and was inhibited by orexigenic ghrelin [25]. | |||||||||||||||
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General Comments
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