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)

Influences of the sympatho-adrenal system on basal and stimulated insulin secretion were studied in vivo in the conscious mouse and rat. In the mouse, adrenalectomy or chemical sympathectomy, induced by 6-hydroxydopamine, lowered basal insulin concentrations moderately. A marked depression of basal insulin concentration (about 50%) was seen after the combined treatment of chemical sympathectomy and adrenalectomy. In short-term experiments in mice, insulin secretion stimulated by glucose or the cholinergic agonist carbachol was enhanced after chemical sympathectomy and/or adrenalectomy, whereas insulin release induced by the synthetic octapeptide of cholecystokinin (CCK-8) was inhibited. The promoting influences on the insulin secretory response to carbachol displayed a rapid development whereas those to glucose developed more slowly. In contrast, the inhibiting effect on CCK-8 stimulated insulin release vanished with time. The insulin secretory response to the beta 2-adrenoceptor stimulator, terbutaline, was increased after chemical sympathectomy, unaffected by adrenalectomy, and decreased after chemical sympathectomy plus adrenalectomy. The glucose elimination rate after 6 weeks of chemical sympathectomy was increased in mice and decreased in rats. The insulin secretory response to glucose was enhanced in mice, whereas it tended to diminish in rats after long-term sympathectomy. In conclusion, the sympatho-adrenal system is involved in regulation of basal insulin concentrations in the mouse, and apparently is of great importance for stimulated insulin secretion; the influence being dependent on the nature of the secretagogue.
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PMID:Adrenalectomy and chemical sympathectomy by 6-hydroxydopamine. Effects on basal and stimulated insulin secretion. 626 83

Vasoactive intestinal peptide (VIP) and cholecystokinin (CCK) have been measured, by radioimmunoassay, in cerebral cortex obtained at autopsy from patients without neurological or psychiatric disease and from patients with Alzheimer's disease, depression and schizophrenia. Sephadex gel filtration indicated that over 90% of the CCK immunoreactivity was associated with the octapeptide in extracted material from the different clinical groups investigated. There were no significant differences from the normal in the overall concentrations of either VIP or CCK in any of the psychiatric groups examined, although differences in Alzheimer's disease were apparent when cases were grouped according to postmortem delay.
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PMID:Neuropeptides in Alzheimer's disease, depression and schizophrenia. A post mortem analysis of vasoactive intestinal peptide and cholecystokinin in cerebral cortex. 626 60

The effect of intrathecal injections of morphine and the two peptides, caerulein and cholecystokinin octapeptide (CCK-8), on the activity in ascending axons of the spinal cord evoked by electrical stimulation of primary nociceptive afferents was studied in spinal rats with decerebration. Morphine (20 microgram) depressed the spontaneous activity and the activity evoked from either A delta-or C-fibres. The co-activation by A delta-fibre stimulation of ascending axons activated by stimulation of C-fibres and the activity in ascending axons activated by stimulation of afferent A beta-fibres were not influenced by morphine. C-Fibre-evoked ascending activity was also depressed by morphine (10 microgram and 5 microgram). Ascending nociceptive activity was not changed by caerulein (30 ng) and CCK-8 300 ng, but it was depressed by a subsequent injection of morphine (20 microgram). The depressant effects of morphine were abolished by an intravenous injection of concluded that: (i) an intrathecal injection of morphine selectively depressed the ascending nociceptive activity; (ii) the depression produced by morphine is an equivalent for spinal analgesia following intrathecal injection of morphine to man; and (iii) the two components of the spinal nociceptive system, the motor and the sensory path, can independently be influenced by drugs.
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PMID:Analgesic effect of intrathecal morphine demonstrated in ascending nociceptive activity in the rat spinal cord an in effectiveness of caerulein and cholecystokinin octapeptide. 627 33

The close relationship of cholecystokinin peptides with some of the dopamine pathways and the limbic system suggests a putative role for these peptides in the pathophysiology of neuropsychiatric disorders such as Parkinson's disease, manic-depression and schizophrenia. By use of radioimmunoassay, we report a significant decrease in cholecystokinin-immunoreactivity in the cerebrospinal fluid of patients with bipolar manic-depression and untreated schizophrenia in comparison to control subjects.
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PMID:Reduced cholecystokinin immunoreactivity in the cerebrospinal fluid of patients with psychiatric disorders. 669 11

In eight volunteers the effect of pentagastrin (0.15, 1.0 and 6.0 microgram/kg body weight/h), secretin (0.5 and 1.0 clinical units/kg b.w./h), and cholecystokinin (CCK) (0.5 and 1.0 Ivy dog units/kg b.w./h) on the gastric secretion of pepsin was investigated to ascertain whether interaction occurred. A high intraindividual variation was found, and also a significant washout of pepsin in the initial period after stimulation. Pepsin secretion was stimulated after pentagastrin (50% above basal level) and even more after secretin (75%-200% above basal level), whereas no stimulation but a tendency for depression was seen after CCK. With the doses of gastrointestinal hormones used in this investigation, no interaction between secretin and CCK on gastric secretion of pepsin in man was demonstrated.
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PMID:Effect of Pentagastrin, secretin, and cholecystokinin on gastric secretion of pepsin in man. 679 45

Intravenous doses of 0.5-8 micrograms/kg (0.3-4.9 nmol/kg) of caerulein, a cholecystokinin-related peptide, depressed the crossed extensor reflex response of chloralose-anesthetized rats in a dose-dependent manner. Intraventricularly administered caerulein was effective only at high doses (1-2 micrograms/animal, i.e., 0.6-1.2 nmol/animal). Cervical vagotomy completely abolished the inhibitory effect of peripherally injected caerulein. Electrical stimulation of vagal afferent nerves could simulate the caerulein effect to some extent. These results suggest that the primary site of action of peripherally administered caerulein is located in the gastrointestinal tract and thus the generated afferent vagal impulses mediate the reflex depression via the nucleus tractus solitarius and other as yet unclarified brain stem structures.
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PMID:Caerulein, a cholecystokinin-related peptide, depresses somatic function via the vagal afferent system. 688 61

1. According to a currently popular biological hypothesis schizophrenic symptoms are caused by a hyperactivity in dopaminergic neurotransmission. Since cholecystokinin (CCK) is a neuromodulator of dopaminergic neurotransmission, the effects of CCK (0.3 microgram/kg; given in a single dose intravenously) were studied in six chronic paranoid schizophrenic patients. 2. Following 3 baseline assessments on separate days, the effects of CCK treatment were assessed immediately after the injection, daily for one week and weekly thereafter for 5 weeks by the Brief Psychiatric Rating Scale (BPRS) and by the Schizophrenia Subscale of the Present State Examination (SS-PSE). 3. One way analysis of variance revealed statistically significant changes in all BPRS factors as well as in the nuclear syndrome and in the total score of the SS-PSE. Dunnett's tests revealed that the time at which the changes from baseline became statistically significant was as follows: anxiety-depression factor of the BPRS, immediately after the injection; anergia factor of the BPRS, by day 2; thought disturbance factor of the BPRS, immediately after; activation factor of the BPRS, immediately after; hostile-suspiciousness factor of the BPRS, by day 1; total BPRS score, immediately after; nuclear syndrome of the SS-PSE, by day 1; and total score of the SS-PSE, by day 1. 4. It is concluded that further controlled studies of the antipsychotic properties of CCK are warranted.
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PMID:Cholecystokinin appears to have antipsychotic properties. 689 17

The serotoninergic neuronal systems of the brain stem are involved in several processes, like sleep, anxiety and depression. Because of this, these systems have received a great deal of attention during the last few years. As a result, the raphe nuclei have been shown to contain a variety of substances in addition to serotonin. For example they were shown to contain GABA, noradrenaline, enkephalin, somatostatin, substance P and cholecystokinin. Additionally, neuropeptide Y and tirotrophine releasing factor have been found to colocalize with serotonin in the dorsal raphe nuclei. All these results have expanded our knowledge on the raphe nuclei and suggest that many other substances, apart from serotonin, could be involved in the regulation of processes such as sleep, anxiety and depression. Further experiments are necessary to test if this hypothesis is correct.
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PMID:[New concepts relating to histochemistry of the serotonergic neural systems of the raphe nucleus]. 748 82

The activity of a selective cholecystokinin (CCK)-A receptor agonist, N-acetyl derivative of A71623 (Ac-Trp-Lys(epsilon-N-[2-methylphenylamino-carbonyl]) -Asp-(NMe)Phe-NH2) was investigated in the guinea pig isolated ileum longitudinal muscle myenteric plexus. NAA caused both a phasic and tonic contraction at all concentrations tested (1-1000 nM). The selective CCK-A antagonist L-364,718 (Devazepide) antagonized both types of contraction with a pKB of 10.10 and 9.95, respectively. The CCK-B selective antagonist L-365,260 ((3R(+)-2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1, 4-benzodiazepine-3yl)-N-(3-methylphenyl)-urea) was inactive up to a concentration of 30 nM. Atropine at 300 nM and 1000 nM reduced the maximal response of NAA by only 17% and 50%, respectively. The selective neurokinin (NK)-1 antagonists GR 82334 ([D-pro9[Spiro-gamma-Lactam] Leu10, Trp11]-Phys (1-11)9) at 300 and 1000 nM and (+-) CP-96,345 [(2S, 3S)-cis- 2-(diphenylmethyl)-N- [(2-methoxyphenyl)-methyl] -1-azabici-clo [2.2.2]octan-3-amine] at 10 nM were inactive or partially active. When atropine and GR 82334 or (+/-) CP-96,345 were combined, they produced a dose-dependent synergistic inhibition of both phasic and tonic contractions induced by NAA. The selective NK-3 receptor agonist senktide induced both phasic and tonic contractions that were blocked by tetrodotoxin. In the presence of atropine and GR 82334, both 300 nM, a synergistic depression of the response to senktide similar to that observed for the agonist NAA was disclosed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A further analysis of the contraction induced by activation of cholecystokinin A receptors in guinea pig isolated ileum longitudinal muscle-myenteric plexus. 752 Sep 41

Selective CCKA and CCKB receptor agonists and antagonists were used to study the involvement of endogenous cholecystokinin in the behavioural changes that occur in mice in the forced-swimming test (Porsolt's test). The CCKB receptor antagonist, L-365,260 ((3R)-(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4- benzodiazepin-3-yl)-3-methylphenylurea), but not the CCKA receptor antagonist, devazepide ((3S)-(-)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepin -3-yl)- 1H-indole-2-carboxamide), elicited an antidepressant-type response (a decrease in the duration of immobility) that was suppressed by previous treatment with either CCK-8 (H-Asp-Tyr(OSO3H)-Met-Gly- Trp-Met-Asp-Phe-NH2) or the selective CCKB receptor agonist BC-264 (Boc-Tyr(SO3H)-gNle-mGly-Trp-N(Me)-Nle-Asp-Phe- NH2). The L-365,260 effect was also prevented by the dopamine receptor antagonist, SCH-23,390 (a dopamine D1-selective receptor antagonist: R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl- 2,3,4,5-tetrahydro-1H-3-benzazepine) and sulpiride (a dopamine D2-selective receptor antagonist: (-)-5-(aminosulfonyl)-N-[(1-ethyl-2-pyrrolidinyl) methyl]-2-metoxybenzamide). On the other hand, co-administration of subthreshold doses of L-365,260 and nomifensine (an atypical antidepressant that selectively blocks dopamine re-uptake mechanisms, 1,2,3,4-tetrahydro-2-methyl-4-phenyl-8-isoquinolinamine) led to a potent antidepressant-type response. These results indicate that blocking of CCKB receptors could result in an increase of extracellular dopamine contents in some brain areas involved in depression and suggest a potential use of CCKB receptor antagonists, alone or combined with antidepressants, in the treatment of depressive syndromes.
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PMID:The CCKB receptor antagonist, L-365,260, elicits antidepressant-type effects in the forced-swim test in mice. 781 46


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