Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Benzodiazepines, chlordiazepoxide and diazepam reversed the antinociceptive action of caerulein in mice. Benzodiazepines (1-5 mg/kg) were administered intraperitoneally and 100 ng of caerulein was injected intracisternally to mice. Benzodiazepines did not change the basal pain threshold of mice but significantly antagonized the antinociceptive effect of caerulein. Proglumide (200 mg/kg, i.p.), which has been claimed to be a specific cholecystokinin receptor antagonist, could also antagonize the antinociceptive effects of caerulein. Naloxone (5 mg/kg) partially but significantly antagonized the antinociceptive effect of caerulein, suggesting that one of the mechanisms of antinociceptive action of caerulein is related to endogenous opioid peptides since benzodiazepines do not act on opioid receptors. Benzodiazepines may decrease the antinociceptive effect of caerulein through acting on cholecystokinin receptors in the central nervous system.
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PMID:Reversal of antinociceptive effect of caerulein by benzodiazepine. 287 7

In mice, intraperitoneally injected chlordiazepoxide and proglumide, both of which are regarded as cholecystokinin (CCK) receptor antagonists in the peripheral tissues, dose-dependently inhibited the satiety induced by 200 ng of intracisternally administered CCK octapeptide (CCK8). Intraperitoneally administered diazepam (1 mg/kg) and/or Ro 15-1788 (5 mg/kg), a benzodiazepine antagonist, both prevented the elevation in the pain threshold induced by 1 microgram of CCK8. However, Ro 15-1788 did not antagonize the effect of diazepam that reversed the CCK-induced antinociception. Ro 15-1788 also inhibited the satiety induced by CCK8. From these results, it was considered that the antagonism, which was observed in the present work, of benzodiazepines and proglumide to CCK8 seemed to occur at the CCK receptor and not at the benzodiazepine receptor in the brain.
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PMID:Possible involvement of the CCK receptor in the benzodiazepine antagonism to CCK in the mouse brain. 288 34

The behavioral and biochemical effects of intracerebroventricular administration of cholecystokinin were investigated in experiments on male Wistar rats. Cholecystokinin induced specific dose-dependent changes in the behavior of the animals. At low doses the inhibiting influence on behavior predominated; at high doses stereo-typed behavior, shaking of the head and increased reactivity to pain stimuli were observed. Cholecystokinin appreciably inhibited the circulation of serotonin and dopamine in the brain structures in comparison with physiological saline solution. Administration of cholecystokinin against a background of phenamine and 5-hydroxy-tryptophan briefly entirely inhibited the behavioral effects induced by these substances. On the basis of the data obtained it can be assumed that cholecystokinin is an endogenous modulator of the activity of the monoaminergic systems of the brain.
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PMID:Intracerebroventricular administration of cholecystokinin inhibits the activity of the dopaminergic and serotoninergic systems of the brain. 299 47

Since the mid-1970s, evidence has accumulated that cholecystokinin (CCK) has a role as a neuromodulator or neurotransmitter in the central nervous system as well as in the periphery. CCK has been shown to have a variety of effects on gastrointestinal functions and is one of the main candidates for a role as a peripheral negative feedback signal to stop feeding behavior. CCK produces satiety not only in animals but also in man: it reduces appetite and activation arising from the preparation of a meal and inhibits intake of liquid and solid food in both lean and obese subjects. The closely related peptide caerulein has similar effects. The site of action of peripherally administered CCK seems to be on an abdominal organ innervated by gastric vagal branches and relayed to the brain by afferent vagal fibres, since selective gastric vagotomy blocks the satiety effect, but pharmacological antagonism of vagal motor effects or lesions of the ventromedial hypothalamus do not. CCK also may have a role in the regulation of pain perception. In mice, CCK and caerulein were shown to produce a decrement in response to noxious stimulation after peripheral and central administration. In man, caerulein was demonstrated to relieve pain originating from biliary and renal colic as well as from cancer and ischemia. A series of studies in healthy man revealed that caerulein also alleviates experimentally induced cutaneous pain. Data from animal studies suggest that CCK-like peptides not only are able to produce analgesic effects on their own, but also are involved in the modulation of opioid systems mediating analgesia. Further study of these effects of CCK should elucidate the regulatory connections between the life-sustaining functions of feeding and pain sensation.
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PMID:Effects of cholecystokinin and caerulein on human eating behavior and pain sensation: a review. 308 29

Over a 6-year period 264 cholecystokinin (CCK) provocation tests have been performed in 174 patients with undiagnosed right upper quadrant pain. All were carried out by one person (T.W.J.L.) as part of a prospective placebo-controlled crossover study. Following infusion of CCK but not saline, 103 patients developed pain (CCK + ve). These patients were offered cholecystectomy and 90 accepted. Seventy patients developed no pain during either infusion (CCK - ve), and one patient experienced pain with both CCK and saline infusions. Of the 90 patients who underwent cholecystectomy, 81 (90 per cent) have been followed up for a mean of 35 months (range 12 months to 5 1/2 years), 67 per cent have had complete resolution of symptoms and a further 24 per cent have had a marked improvement in symptoms. Only 9 per cent of patients did not benefit from cholecystectomy. This compares well with patients undergoing cholecystectomy for uncomplicated calculous gallbladder disease, 88 per cent of whom, in our study, were improved by surgery. Patients with a positive CCK test have an excellent chance of symptomatic improvement following cholecystectomy.
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PMID:Cholecystokinin (CCK) provocation test: long-term follow-up after cholecystectomy. 231 86

In adult mammals, cholecystokinin (CCK)-opiate interactions are complex and task dependent. Specifically, CCK antagonizes opiate effects in some cases, yet acts similarly to opiate agonists in others. The present study used behavioral measures to determine how CCK interacts with opiates in neonatal rats. CCK, at doses of 1 microgram/kg and higher, markedly reduced isolation-induced distress vocalization in rat pups. Moreover, CCK selectively prevented naltrexone antagonism of opiate-mediated reduction in distress vocalization in 3- and 11-day-old rats. Yet CCK did not affect opiate-induced analgesia, as measured by the hot-plate paw-lift response. Thus CCK either did not interact with opiates or did so agonistically, with the same (low) dose range, and within subjects. These findings suggest independence of stress and pain systems in neonatal rats and demonstrate a functional interaction between CCK and opioid systems.
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PMID:Behavioral evidence for cholecystokinin-opiate interactions in neonatal rats. 320 24

This paper reviews the value of administration of cholecystokinin (CCK) in the assessment of patients thought to have acalculous biliary pain. The literature contains conflicting reports and there is no unequivocal evidence to support the use of CCK provocation tests as a basis for deciding the need for cholecystectomy.
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PMID:Clinical application of the cholecystokinin provocation test. 231 86

The sites of origin of brain stem enkephalin and cholecystokinin projections to the rodent spinal trigeminal nucleus were studied utilizing the combined retrograde transport-peroxidase antiperoxidase immunohistochemical technique. Several brain stem areas were found to contain enkephalin-like immunoreactive double-labeled neurons following injection of wheat germ agglutinin-horseradish peroxidase or horseradish peroxidase into the spinal trigeminal nucleus. The largest numbers of enkephalin double-labeled neurons were identified in the nucleus pontis oralis, nucleus raphe medianis, medial vestibular nucleus and the midbrain periaqueductal gray. Enkephalin projections to the spinal trigeminal nucleus were also found to originate from the nucleus solitarius, nucleus raphe pallidus, nucleus raphe magnus, nucleus raphe dorsalis, nucleus reticularis paragigantocellularis, nucleus reticularis gigantocellularis pars alpha and the deep mesencephalic nucleus. In contrast to the numerous sources of enkephalin input to the spinal trigeminal nucleus, cholecystokinin projections to this region were limited to four brain stem nuclei. These included the nucleus solitarius, raphe obscurus, nucleus paragigantocellularis and the ventral reticular nucleus of the medulla. The finding that only a small number of brain stem cholecystokinin-like immunoreactive neurons project to the spinal trigeminal nucleus supports the hypothesis that most of the cholecystokinin input to the spinal trigeminal nucleus arises from primary afferent trigeminal fibers. The spinal trigeminal nucleus is known to play a role in processing sensory information and in the transmission of orofacial nociception. The present study identifies several brain stem sites which provide enkephalin and/or cholecystokinin input to the spinal trigeminal nucleus. Several of these nuclei have been implicated as components of the endogenous pain control system and the present results raise the possibility that they may modulate incoming orofacial nociception by releasing the endogenous opioid, enkephalin. Cholecystokinin, on the other hand, has been demonstrated in other studies to attenuate the action of opiates and thus may play an opposing role in the spinal trigeminal nucleus.
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PMID:The nuclei of origin of brainstem enkephalin and cholecystokinin projections to the spinal trigeminal nucleus of the rat. 329 85

A study has been made of the involvement of spinal peptidergic neurons in ascending tracts at lumbar-sacral levels in rats, by combining the retrograde transport of a protein-gold complex with immunocytochemistry. Ten neuropeptides have been considered for their presence in the cells of origin of the following six ascending tracts, including some involved in pain transmission: the spinosolitary tract, the medial and lateral spinoreticular tracts, the spinomesencephalic tract, the spinothalamic tract and the postsynaptic dorsal column tract. Although there was overlap in the distribution of several of the types of peptidergic cells and some ascending tract cells only a very small percentage of long ascending tract cells were found to contain neuropeptides. Most (90%) of those peptidergic ascending tract cells, however, were clearly congregated in two distinct spinal regions: the lateral spinal nucleus and the region surrounding the central canal (including lamina X). Ascending tract cells in both of these regions contained a wide variety of neuropeptides. Immunoreactivities for a total of seven different peptides were seen. The lateral spinal nucleus had the highest percentage of neuropeptide containing ascending tract cells; cells of all the four populations of peptidergic neurons lying in this region were involved in supraspinal projections; they stained for vasoactive intestinal polypeptide, bombesin, substance P or dynorphin and their axons projected in the spinomesencephalic, spinoreticular and spinosolitary tracts. The region surrounding the central canal contained bombesin-, enkephalin-, cholecystokinin- and somatostatin-immunoreactive ascending tract cells; these cells were found at the origin of the spinothalamic, spinomesencephalic, spinoreticular and spinosolitary tracts. In this region only the cells staining for substance P were not involved in supraspinal projections. The peptidergic ascending tract cells in other spinal regions were few; they were found in either lamina I or lateral part of lamina V. Ascending tract lamina I cells reacted for dynorphin or vasoactive intestinal polypeptide and their axons projected in the spinosolitary and spinomesencephalic tracts. Ascending tract lamina V cells reacted for somatostatin and were found at the origin of the medial component of the spinoreticular tract. It is proposed that peptidergic ascending tract cells form minor but distinct subgroups within each ascending tract. Each of the ascending tracts are divisible into peptide- and nonpeptide-containing groups of cells which convey information in a parallel fashion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:neuropeptides in long ascending spinal tract cells in the rat: evidence for parallel processing of ascending information. 336 49

Fifteen patients with history of biliary colic, induceable by cholecystokinin, but normal oral cholecystogram and ultrasonogram were studied prior to and after cholecystectomy. Fasting duodenal bile, obtained preoperatively after administration of cholecystokinin, and gallbladder bile obtained at operation were analyzed. The lipid composition as well as the cholesterol saturation were within the range seen in gallstone-free subjects. The total lipid concentration of gallbladder bile was normal, whereas that of duodenal bile was reduced by about 50%, indicating a less efficient gallbladder emptying. In 10 of the 15 patients, the analysis of the excised gallbladder displayed macro- or microscopic abnormalities; two patients had cholesterol gallstones. At re-examination 9-27 months after the operation, 12 of the patients were completely symptom-free and two patients reported a clear improvement while on still had unchanged symptoms. It is concluded that cholecystectomy is the treatment to prefer in patients with "acalculous" biliary pain, induceable by cholecystokinin.
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PMID:Biliary colic without evidence of gallstones: diagnosis, biliary lipid metabolism and treatment. 346 Feb 88


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