Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of several doses of cholecystokinin octapeptide sulphate ester (CCK-8-SE) and nonsulphated cholecystokinin octapeptide (CCK-8-NS), and two CCK-related peptide analogues Ac-Thr5-caerulein, and nonsulphated Ac-Thr5-caerulein were investigated on electroshock-(ES)-induced seizures after intraperitoneal administration in mice. As parameters, the duration of the tonic and clonic phase of the fit, and those of postictal coma and behavioural depression were measured. CCK-8-SE decreased the duration of the clonic phase; its highest dose, 3.2 mumol/kg, shortened the coma. CCK-8-NS antagonized only slightly the clonic phase of seizure. Ac-Thr5-caerulein did not influence ES-induced seizures in any dose, only increased the duration of behavioural depression. Similarly to CCK-8-NS, the nonsulphated form of Ac-Thr5-caerulein inhibited selectively the clonic phase of seizures. The reference drugs, diazepam and phenobarbital, antagonized dose-dependently and most effectively the tonic phase of ES-induced seizures, but in much higher doses than did the CCK-related peptides. Besides, diazepam increased and phenobarbital decreased the duration of postictal coma. The results showed that the tested CCK-related peptides inhibit prevalently the clonic phase of ES-induced seizures after peripheral administration.
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PMID:Inhibition of electroshock-induced seizures by cholecystokinin-related peptides in mice. 359 54

We investigated the effect of chronic intracerebroventricular infusion of the sulfated cholecystokinin octapeptide (CCK-8S) on sleep pattern and respiratory rate. The results indicate a depression of respiratory rate during Non-REM and REM sleep as well as an increase in the number of REM periods occurring per hour of Non-REM sleep. It is suggested that central release of CCK-8S is capable of modulating the automatic regulation of respiration during sleep and altering the normal sleep-waking pattern.
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PMID:Effect of chronic intracerebroventricular infusion of cholecystokinin on respiration and sleep. 374 95

This review examines the various clinical options used to elicit gastric emptying, viz. drug-induced emesis, mechanical pharyngeal stimulation, gastric lavage, and catharsis. Apomorphine and syrup of ipecac are the 2 drugs most frequently used for induction of emesis. Both agents act centrally and, in addition, syrup of ipecac has a peripheral action. Toxins ingested or foods previously eaten may inhibit or enhance emetic action by interfering with mediating and conducting mechanisms. Studies indicate that both syrup of ipecac and apomorphine are similarly effective in inducing emesis; however, apomorphine has a shorter reaction time compared with syrup of ipecac. There are more risks involved with the use of apomorphine, since it causes central nervous system and respiratory depression. Syrup of ipecac has been shown to be relatively safe when used in its recommended dosage for emesis. However, several toxicities have been reported with the use of the fluid extract of ipecac. Emesis is contraindicated in patients who are obtunded or comatose, and in patients who have ingested stimulants, some hydrocarbons, or corrosives. Mechanical pharyngeal stimulation is a simple method of inducing emesis; however, it is often unsuccessful and rarely recovers a significant portion of the gastric contents. Gastric lavage is a procedure which has been relied upon for over a century. Its effectiveness is dependent on the nature, form, and dosage of the poison, latency between time of ingestion and lavage, and technique. In clinical experiments studying gastric lavage, it has been noted that the procedure is most beneficial 1 to 2 hours postingestion for the majority of poison ingestions. Lavage also provides an excellent route for activated charcoal and selected antidotes. Gastric lavage may pose several risks to the patient, including obstruction and contamination of the airways and oesophageal damage. Contraindications for gastric lavage are similar to those for emesis except that it may be safer to use in obtunded, comatose, or uncooperative patients. Cathartics used during initial poisoning therapy are usually the saline cathartics. They elicit an osmotic reaction in the small intestine which results in increased intraluminal fluid bulk, hyperperistalsis, and subsequent propulsion of contents. Cathartics have also been shown to stimulate the secretion of cholecystokinin, which is thought to have similar effects on the intestine. Cathartics have not been shown to significantly enhance drug elimination from the gastrointestinal tract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Gastric emptying. Risk versus benefit in the treatment of acute poisoning. 378 40

In unanesthetized dogs with Heidenhain pouches and separated duodenal pouches, intravenous infusion of commercial cholecystokinin (1.0 IDU per min) produced a significant depression of pouch acid and pepsin secretion stimulated by pentagastrin (1.0 microg per min) or by methacholine (2.0 microg per min). Acid response to methacholine was temporarily augmented. Irrigation of the duodenal pouches with emulsified fat produced similar patterns of depression of acid secretion in response to pentagastrin and pepsin secretion in response to pentagastrin or methacholine. Acid secretion stimulated by methacholine was temporarily augmented after the irrigation. It is concluded that fat releases endogenous cholecystokinin from the duodenal mucosa and that cholecystokinin, or duodenal fat, powerfully depresses Heidenhain pouch pepsin secretion in dogs. The involvment of the gastric inhibitory polypeptide (GIP) cannot be assessed from the present experiments.
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PMID:Inhibition of Heidenhain pouch pepsin secretion by commercial cholecystokinin and duodenal fat in dogs. 460 62

The intrathecal (i.t.) administration of morphine inhibits nociceptive motor responses and activity in ascending axons evoked by stimulation of nociceptive afferent nerve fibers (nociceptive sensory response) in the rat. The i.t. administration of cholecystokinin octapeptide and ceruletide inhibits nociceptive motor responses, but does not affect ascending nociceptive activity. This shows that drug-induced depression of nociceptive motor responses is not always associated with depression of the nociceptive sensory response of the spinal cord. The microiontophoretic application of substance P excites single dorsal horn neurons that respond to noxious stimulation, whereas the i.t. administration of substance P inhibits both nociceptive motor and sensory responses. Thus, the results obtained from the i.t. administration of a drug may differ from those obtained from its application to single spinal neurons. Diazepam inhibits spinal reflexes and may reduce pain sensation in humans. To assess whether a spinal action is involved in the pain-relieving effect of diazepam, experiments were carried out on spinalized rats in which activity evoked by the stimulation of nociceptive and nonnociceptive afferent nerve fibers of the sural nerve was recorded from single ascending axons below the site of spinal cord transection. Diazepam, 20 micrograms i.t., reduced activity evoked by afferent A delta and C fiber stimulation and by stimulation of afferent A beta fibers. The depressant effect caused by diazepam, 2 mg/kg i.v., on C fiber-evoked ascending activity was reduced by the i.t. injection of the benzodiazepine antagonist, Ro 15-1788 (40 micrograms), an imidazodiazepine. It is concluded that the depression by diazepam of C fiber-evoked ascending activity contributes to pain relief caused by the drug.
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PMID:Depression of nociceptive sensory activity in the rat spinal cord due to the intrathecal administration of drugs: effect of diazepam. 609 60

Immunoreactive somatostatin, bombesin, and cholecystokinin were measured in cerebrospinal fluid of normal subjects and patients with anorexia nervosa, depression, mania, and schizophrenia. Somatostatin-like immunoreactivity was decreased in anorexic and depressed patients. Bombesin-like immunoreactivity tended to be decreased in schizophrenics. Cholecystokinin-like immunoreactivity did not differ between groups. These data suggest a possible function for neuropeptides in regulation of human behavior.
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PMID:Altered neuropeptide concentrations in cerebrospinal fluid of psychiatric patients. 612 76

The effect of intraduodenal trypsin activity on pancreatic exocrine secretion was studied in conscious Syrian golden hamsters provided with bile-pancreatic fistulae. The secretion (secretory volume, amylase and protein output) was stable during a collection period of 14 h without any duodenal infusions. Infusion into the duodenum of bicarbonate or bile did not affect the secretion. When, however, bile-pancreatic juice or trypsin was administered intraduodenally, a marked depression of amylase and protein output was found. After addition of trypsin inhibitor--in a dose sufficient to eliminate all trypsin activity--to either of the two infusates the secretion was restored to the initial values. In a long-term experiment (10 days) repeated subcutaneous injections of cholecystokinin caused a significant increase of pancreatic protein and amylase content in the hamster. Oral trypsin inhibitor administration for 10 days had similar, although not so pronounced effects. Subcutaneous secretin administration was without effect in this respect. The results show that pancreatic enzyme secretion in the Syrian golden hamster is controlled by a negative feedback regulation exerted by intraluminal trypsin. The findings also suggest that both cholecystokinin and orally administered trypsin inhibitor exert trophic effects on the pancreas.
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PMID:Regulatory effects on the pancreas of intraduodenal pancreatic juice and trypsin in the Syrian golden hamster. 620 95

Strips of muscularis mucosae from the oesophagi of cat, dog and opossum have been studied to determine their responses to drugs to electrical field stimulation. All tissues were contracted by acetylcholine, histamine and, with the exception of strips of muscularis mucosae from the opossum proximal oesophagus, noradrenaline. The effects of acetylcholine and histamine were competitively antagonized by atropine (50 nM) and mepyramine (50 nM) and were abolished by atropine (1 microM) and mepyramine (1 microM) respectively. Contractile responses to noradrenaline were competitively antagonized by phentolamine (50 nM) but were converted to propranolol (50 nM)-sensitive relaxations by phentolamine (1 microM). Relaxations were abolished by propranolol (1 microM). Cholecystokinin octapeptide, gastrin 1 and vasoactive intestinal polypeptide were ineffective on any of the tissues examined. Substance P caused contractions in tissue from all three species. These effects were atropine and tetrodotoxin insensitive. All tissues gave atropine (50 nM)- and tetrodotoxin (100 nM)-sensitive contractions in response to electrical field stimulation. Contractions were not followed by relaxations and spontaneous mechanical activity was not suppressed between periods of stimulation. No evidence was obtained for the presence of non-adrenergic, non-cholinergic inhibitory innervation of the oesophageal muscularis mucosae in any species. During electrical field stimulation noradrenaline always reduced the amplitude of evoked contractions and, with the exception of tissue from proximal opossum oesophagus, increased resting tension. In opossum distal oesophageal muscularis mucosae, the effects of noradrenaline during electrical field stimulation were abolished by a 30 min pretreatment of the tissue with phentolamine (1 microM) and propranolol (1 microM). To Achieve this in all other tissues, it was also necessary to use yohimbine (1 microM). 7 In all tissues where noradrenaline caused a phentolamine (1 microM)-and propranolol (1 microM)- resistant depression of electrically evoked responses, clonidine produced a yohimbine (1 microM)- sensitive depression. 8 Evidence was obtained for the presence of excitatory alpha 1-and inhibitory alpha 2- and beta-adrenoceptors. Inter-species differences in their distribution are discussed.
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PMID:A pharmacological study of oesophageal muscularis mucosae from the cat, dog and American opossum (Didelphis virginiana). 620 83

Vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK) and gastrin in the cerebrospinal fluid (CSF) were studied in patients with endogenous depression, non-endogenous depression, mania, schizophrenia and a control group. All patients were classified according to ICD-9 and the group of depressions was further classified according to the Newcastle Rating Scales for depression (Carney et al. 1965) (N-I). In the group of non-endogenously depressed patients, CSF-VIP levels (median 16 pmol/l) were found to be significantly lower than those of controls (median = 32 pmol/l) and endogenous depressives (36 pmol/l). In the non-endogenous group, it appeared that the low CSF-VIP was due to a group of patients who, during a past or present depressive episode, had been diagnosed as suffering from endogenous depression. Moreover, this group was clinically characterized by 'dysphoric/hysterical features', 'reversed diurnal variation' (i.e. worse in the evening), and 'lack of clearly circumscribed episodes'. In many aspects this group seems similar to the atypical depressives described as monoamine oxidase inhibitor responders. Concerning CSF-CCK and CSF-gastrin, no significant differences between the examined groups were demonstrated.
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PMID:Vasoactive intestinal polypeptide decreased in cerebrospinal fluid (CSF) in atypical depression. Vasoactive intestinal polypeptide, cholecystokinin and gastrin in CSF in psychiatric disorders. 624 Dec 14

Twenty-three pigs, 1-3 mo of age, were fitted variously with intraperitoneal, intrajugular, intraportal, and intraduodenal catheters. After a 4-h fast, porcine cholecystokinin (CCK), 5-40 Ivy dog units/kg body wt (IDU/kg); caerulein, 0.25-2 micrograms/kg; or the octapeptide of cholecystokinin (CCK-OP), 5-40 IDU/kg, was given parenterally; or 2-5% sodium oleate or 5% protein hydrolysate (5 ml/kg) was injected intraduodenally. Pelleted feed intake was then measured for 10 min. Food intake was depressed in a dose-related fashion in all instances as compared to after 0.9% NaCl control injections. For example, feed consumption following 5 and 40 IDU/kg of CCK intrajugularly was 84 +/- 2 and 6 +/- 4 (SE) %, respectively, of control intake. Intraportal infusion produced a greater depression of feeding. A conditioned taste aversion could not be formed to CCK, caerulein, or CCK-OP. Sodium oleate or protein hydrolysate, releasers of endogenous CCK, depressed feeding, and this satiety effect was attenuated when given with 0.5% tetracaine. The results support the hypothesis that CCK participates in rapid, presumably preabsorptive, satiety.
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PMID:Cholecystokinin and satiety in pigs. 626 13


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