PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30147637-1 2018 Studies demonstrated that cholecystokinin (CCK) system involved in morphine dependence and withdrawal. Morphine 67-75 cholecystokinin Homo sapiens 26-41 30147637-1 2018 Studies demonstrated that cholecystokinin (CCK) system involved in morphine dependence and withdrawal. Morphine 67-75 cholecystokinin Homo sapiens 43-46 30147637-2 2018 Our previous study showed that endogenous CCK system were up-regulated after chronic morphine exposure. Morphine 85-93 cholecystokinin Homo sapiens 42-45 30147637-3 2018 Additionally, CCK1 receptor significantly blocked the inhibitory effect of exogenous CCK-8 on morphine dependence, but CCK2 receptor appears to be necessary for low concentrations of endogenous CCK to potentiate morphine dependence. Morphine 94-102 cholecystokinin Homo sapiens 14-17 30147637-3 2018 Additionally, CCK1 receptor significantly blocked the inhibitory effect of exogenous CCK-8 on morphine dependence, but CCK2 receptor appears to be necessary for low concentrations of endogenous CCK to potentiate morphine dependence. Morphine 94-102 cholecystokinin Homo sapiens 85-88 22682150-1 2012 BACKGROUND: Cholecystokinin octapeptide (CCK-8), the most potent endogenous anti-opioid peptide, has been shown to regulate the processes of morphine dependence. Morphine 141-149 cholecystokinin Homo sapiens 12-27 22682150-0 2012 Cholecystokinin receptor-1 mediates the inhibitory effects of exogenous cholecystokinin octapeptide on cellular morphine dependence. Morphine 112-120 cholecystokinin Homo sapiens 0-15 22682150-0 2012 Cholecystokinin receptor-1 mediates the inhibitory effects of exogenous cholecystokinin octapeptide on cellular morphine dependence. Morphine 112-120 cholecystokinin Homo sapiens 72-87 22682150-1 2012 BACKGROUND: Cholecystokinin octapeptide (CCK-8), the most potent endogenous anti-opioid peptide, has been shown to regulate the processes of morphine dependence. Morphine 141-149 cholecystokinin Homo sapiens 41-44 22682150-5 2012 The CCK receptor and endogenous CCK were up-regulated after chronic morphine exposure. Morphine 68-76 cholecystokinin Homo sapiens 4-7 22682150-5 2012 The CCK receptor and endogenous CCK were up-regulated after chronic morphine exposure. Morphine 68-76 cholecystokinin Homo sapiens 32-35 22682150-7 2012 Interestingly, CCK-8 (0.1-1 muM), a strong CCK receptor agonist, dose-dependently inhibited the naloxone-precipitated cAMP overshoot in SH-SY5Y cells when co-pretreated with morphine. Morphine 174-182 cholecystokinin Homo sapiens 15-18 22682150-9 2012 Therefore, the CCK2 receptor appears to be necessary for low concentrations of endogenous CCK to potentiate morphine dependence in SH-SY5Y cells. Morphine 108-116 cholecystokinin Homo sapiens 15-18 22682150-11 2012 CONCLUSIONS: This study reveals the difference between exogenous CCK-8 and endogenous CCK effects on the development of morphine dependence, and provides the first evidence for the participation of the CCK1 receptor in the inhibitory effects of exogenous CCK-8 on morphine dependence. Morphine 120-128 cholecystokinin Homo sapiens 65-68 22682150-11 2012 CONCLUSIONS: This study reveals the difference between exogenous CCK-8 and endogenous CCK effects on the development of morphine dependence, and provides the first evidence for the participation of the CCK1 receptor in the inhibitory effects of exogenous CCK-8 on morphine dependence. Morphine 120-128 cholecystokinin Homo sapiens 86-89 22682150-11 2012 CONCLUSIONS: This study reveals the difference between exogenous CCK-8 and endogenous CCK effects on the development of morphine dependence, and provides the first evidence for the participation of the CCK1 receptor in the inhibitory effects of exogenous CCK-8 on morphine dependence. Morphine 120-128 cholecystokinin Homo sapiens 86-89 20547453-1 2010 It has been known that co-administration of morphine with either cholecystokinin (CCK) receptor or melanocortin (MC) receptor antagonists enhance morphine"s analgesic efficacy by reducing serious side effects such as tolerance and addiction. Morphine 44-52 cholecystokinin Homo sapiens 65-80 20547453-1 2010 It has been known that co-administration of morphine with either cholecystokinin (CCK) receptor or melanocortin (MC) receptor antagonists enhance morphine"s analgesic efficacy by reducing serious side effects such as tolerance and addiction. Morphine 44-52 cholecystokinin Homo sapiens 82-85 20547453-1 2010 It has been known that co-administration of morphine with either cholecystokinin (CCK) receptor or melanocortin (MC) receptor antagonists enhance morphine"s analgesic efficacy by reducing serious side effects such as tolerance and addiction. Morphine 146-154 cholecystokinin Homo sapiens 65-80 20547453-1 2010 It has been known that co-administration of morphine with either cholecystokinin (CCK) receptor or melanocortin (MC) receptor antagonists enhance morphine"s analgesic efficacy by reducing serious side effects such as tolerance and addiction. Morphine 146-154 cholecystokinin Homo sapiens 82-85 11432973-0 2001 Morphine-induced in vivo release of spinal cholecystokinin is mediated by delta-opioid receptors--effect of peripheral axotomy. Morphine 0-8 cholecystokinin Homo sapiens 43-58 17196636-0 2006 Cholecystokinin is necessary for the expression of morphine conditioned place preference. Morphine 51-59 cholecystokinin Homo sapiens 0-15 17196636-6 2006 These results indicate that endogenous CCK modulates the incentive-salience of morphine-associated cues and suggest that CCK antagonists may be useful in the treatment of drug craving. Morphine 79-87 cholecystokinin Homo sapiens 39-42 16686530-2 2006 CCK may be upregulated in conditions of chronic pain or during sustained morphine administration resulting in attenuation of opioid-mediated pain relief. Morphine 73-81 cholecystokinin Homo sapiens 0-3 11432973-1 2001 Morphine and other opioid agonists induce spinal in vivo release of cholecystokinin (CCK), a neuropeptide with anti-opioid properties. Morphine 0-8 cholecystokinin Homo sapiens 68-83 11432973-1 2001 Morphine and other opioid agonists induce spinal in vivo release of cholecystokinin (CCK), a neuropeptide with anti-opioid properties. Morphine 0-8 cholecystokinin Homo sapiens 85-88 11432973-3 2001 In the present in vivo microdialysis study, the morphine-induced release of cholecystokinin-like immunoreactivity (CCK-LI) in the dorsal horn was completely blocked by the delta-opioid antagonist naltrindole (10 microM in the perfusion fluid). Morphine 48-56 cholecystokinin Homo sapiens 76-91 11432973-3 2001 In the present in vivo microdialysis study, the morphine-induced release of cholecystokinin-like immunoreactivity (CCK-LI) in the dorsal horn was completely blocked by the delta-opioid antagonist naltrindole (10 microM in the perfusion fluid). Morphine 48-56 cholecystokinin Homo sapiens 115-118 11432973-11 2001 The present data indicate that the delta-opioid receptor mediates morphine-induced CCK-LI release in the spinal cord. Morphine 66-74 cholecystokinin Homo sapiens 83-86 2694075-12 1989 Accordingly, others have found that small (and most probably, physiological) doses of CCK-8 attenuate the analgesic effects of morphine, and of endogenous opioids. Morphine 127-135 cholecystokinin Homo sapiens 86-89 9806692-0 1998 The cholecystokinin antagonist proglumide enhances the analgesic efficacy of morphine in humans with chronic benign pain. Morphine 77-85 cholecystokinin Homo sapiens 4-19 9806692-12 1998 In this study, we demonstrated that the cholecystokinin antagonist proglumide increases the analgesic effect of morphine in some patients with chronic benign pain. Morphine 112-120 cholecystokinin Homo sapiens 40-55 9098217-10 1997 Morphine augmentation significantly increased the frequency of gallbladder visualization in patients pretreated with CCK. Morphine 0-8 cholecystokinin Homo sapiens 117-120 9098218-8 1997 suggest that morphine augmentation can further improve the efficacy of the test even after CCK pretreatment. Morphine 13-21 cholecystokinin Homo sapiens 91-94 8713957-4 1995 Oxytocin release following CCK (and that during parturition) is potently inhibited by morphine, which blocks the local noradrenaline release in the supraoptic nucleus. Morphine 86-94 cholecystokinin Homo sapiens 27-30 2364292-14 1990 morphine antinociception, chronic treatment causes loss of facilitation or attenuation of opioid antinociception, suggesting that (1) compensatory alterations in CCK-opioid interactions develop during chronic CCK blockade and (2) CCK antagonists may not be useful adjuncts to opioid analgesics in the management of chronic pain in man. Morphine 0-8 cholecystokinin Homo sapiens 162-165 2364292-14 1990 morphine antinociception, chronic treatment causes loss of facilitation or attenuation of opioid antinociception, suggesting that (1) compensatory alterations in CCK-opioid interactions develop during chronic CCK blockade and (2) CCK antagonists may not be useful adjuncts to opioid analgesics in the management of chronic pain in man. Morphine 0-8 cholecystokinin Homo sapiens 209-212 2364292-14 1990 morphine antinociception, chronic treatment causes loss of facilitation or attenuation of opioid antinociception, suggesting that (1) compensatory alterations in CCK-opioid interactions develop during chronic CCK blockade and (2) CCK antagonists may not be useful adjuncts to opioid analgesics in the management of chronic pain in man. Morphine 0-8 cholecystokinin Homo sapiens 209-212 1589765-0 1992 Cholecystokinin antianalgesia: safety cues abolish morphine analgesia. Morphine 51-59 cholecystokinin Homo sapiens 0-15 1628146-15 1992 Application of CCK antagonists may be clinically important in treating chronic pain patients by preventing morphine tolerance and by eliminating the need to increase morphine doses to unacceptable levels. Morphine 107-115 cholecystokinin Homo sapiens 15-18 1628146-15 1992 Application of CCK antagonists may be clinically important in treating chronic pain patients by preventing morphine tolerance and by eliminating the need to increase morphine doses to unacceptable levels. Morphine 166-174 cholecystokinin Homo sapiens 15-18 2364292-0 1990 Chronic administration of cholecystokinin antagonists reverses the enhancement of spinal morphine analgesia induced by acute pretreatment. Morphine 89-97 cholecystokinin Homo sapiens 26-41 2979238-1 1988 In an attempt to find the ideal analgesic to treat biliary tract pain we compared the effects of saline and equianalgesic doses of morphine, pentazocine, pethidine, and butorphanol on CCK-OP stimulated gallbladder emptying in healthy volunteers. Morphine 131-139 cholecystokinin Homo sapiens 184-187 3838690-0 1985 Potentiation of morphine analgesia by the cholecystokinin antagonist proglumide. Morphine 16-24 cholecystokinin Homo sapiens 42-57 3656653-0 1987 [Cholecystokinin antagonist (proglumide) potentiates the inhibitory effect of morphine on micturition reflex]. Morphine 78-86 cholecystokinin Homo sapiens 1-16 3697717-2 1986 The present study determined the effects of various levels of morphine treatment on hypothalamic levels of CCK as determined by radioimmunoassay. Morphine 62-70 cholecystokinin Homo sapiens 107-110 3697717-3 1986 Acute treatment with morphine sulfate (10 mg/kg) or implantation of one morphine pellet (75 mg free base) increased levels of CCK in whole hypothalamus. Morphine 21-37 cholecystokinin Homo sapiens 126-129 3697717-3 1986 Acute treatment with morphine sulfate (10 mg/kg) or implantation of one morphine pellet (75 mg free base) increased levels of CCK in whole hypothalamus. Morphine 21-29 cholecystokinin Homo sapiens 126-129 3697717-5 1986 In samples dissected into hypothalamic subregions, the effect of morphine on CCK levels was localized to medial but not lateral or posterior regions. Morphine 65-73 cholecystokinin Homo sapiens 77-80 4014744-0 1985 Potentiation of systemic morphine analgesia in humans by proglumide, a cholecystokinin antagonist. Morphine 25-33 cholecystokinin Homo sapiens 71-86 3838691-1 1985 We have recently observed that exogenous sulfated cholecystokinin octapeptide (CCK) can antagonize various forms of opiate analgesia and that the CCK receptor blocker proglumide potentiates morphine analgesia. Morphine 190-198 cholecystokinin Homo sapiens 146-149 6294831-1 1983 The endogenous neuropeptide cholecystokinin, when administered systemically or perispinally, potently antagonizes opiate analgesia produced by foot shock and morphine. Morphine 158-166 cholecystokinin Homo sapiens 28-43 6184121-6 1982 The potassium-stimulated release of SP and CCK was profoundly depressed by the addition of morphine (10(-5) M) in a naloxone-reversible manner. Morphine 91-99 cholecystokinin Homo sapiens 43-46 3861127-3 1985 Systemic administration of CCK attenuated opiate analgesias produced by morphine and footshock, but did not reduce nonopiate footshock analgesia. Morphine 72-80 cholecystokinin Homo sapiens 27-30 3861127-5 1985 Sequestering of endogenously circulating CCK by antibodies raised against CCK through an active immunization procedure resulted in a potentiation of morphine analgesia. Morphine 149-157 cholecystokinin Homo sapiens 41-44 3861127-5 1985 Sequestering of endogenously circulating CCK by antibodies raised against CCK through an active immunization procedure resulted in a potentiation of morphine analgesia. Morphine 149-157 cholecystokinin Homo sapiens 74-77 6198038-4 1984 The IC50 of naloxone for the antagonism by DADL and morphine of the release of CCK were similar, whereas the naloxone IC50 was lower for morphine than DADL in the reversal of the effects of the agonist in sP release. Morphine 52-60 cholecystokinin Homo sapiens 79-82