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)

1. Responses of cerebral cortical neurones to the microiontophoretic application of acetylcholine, noradrenaline, cyclic adenosine 3',5'-monophosphate (cyclic AMP) and cyclic guanosine 3',5'-monophosphate (cyclic GMP) were examined.2. The application of acetylcholine and cyclic GMP to identified pyramidal tract neurones resulted in an increased frequency of firing in a large number of cells. Upon application of both substances to cells which could not be identified as pyramidal tract cells, a reduction in the frequency of spontaneous firing was sometimes observed.3. Careful current controls had no effect on the cells discussed here, indicating that the observed responses were not due to the iontophoretic currents. Also, the electro-osmotic ejection of cyclic GMP (outward current) produced similar changes of cell firing to those which followed iontophoretic application (inward current).4. The microiontophoretic application of atropine resulted in a blockade of acetylcholine responses while leaving responses to cyclic GMP unaffected. This suggests that cyclic GMP was not acting indirectly by releasing acetylcholine from presynaptic endings.5. Ejection of cyclic GMP from solutions containing calcium ions produced responses comparable to those produced by cyclic GMP alone. It is unlikely therefore that cyclic GMP was causing excitation by chelating calcium.6. Applications of noradrenaline and cyclic AMP produced a reduction in the spontaneous discharge rate of most neurones tested.7. Phosphodiesterase inhibitors such as ICI 63,197 caused a potentiation of the noradrenaline responses of pyramidal tract neurones.8. 5'-adenosine monophosphate produced a powerful depression of all cells to which it was applied. This action was blocked by aminophylline, suggesting the effect was mediated through an adenosine receptor. Responses to cyclic AMP were usually not abolished, but were reduced by about 50% in amplitude.9. These results are consistent with the hypothesis that cyclic AMP may mediate some neuronal effects of noradrenaline and cyclic GMP may mediate some effects of acetylcholine. The results are also consistent with the suggestion that the two nucleotides may sometimes mediate opposite cellular responses to humoral stimuli.
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PMID:Microiontophoretic studies of the effects of cylic nucleotides on excitability of neurones in the rat cerebral cortex. 19 28

Heavy metal treatment (2 X 1 mg/kg per day) for 3, 5, and 7 days resulted in progressive augmentation in the incorporation of [14C]thymidine into hepatic DNA. In contrast with the observed enhancement in DNA synthesis, cadmium exposure tended to produce a decrease in the activity of hepatic ornithine decarboxylase (EC 4.1.1.17) at 1, 3, or 5 days with the lowest (34% of control values) enzymic activity seen after 7 days. A similar reduction in the activity of S-adenosylmethionine decarboxylase (EC 4.1.1.50) was observed in livers of rats treated with cadmium for 1-7 days. Subacute exposure to cadmium significantly lowered the hepatic levels of spermidine and spermine whereas the endogenous concentrated of putrescine remained unaltered. In addition to the observed effects on the biosynthesis of polyamines and DNA, heavy metal treatment produced stimulation of the hepatic adenylate cyclase (EC 4.6.1.1)--cyclic AMP system. Significant increases in the activity of hepatic adenylate cyclase and endogenous cyclic AMP levels were detected as early as 1 day and the observed alterations persisted during the entire 1-week period of cadmium exposure. The depression in polyamine formation was accompanied by enhanced DNA biosynthesis as well as stimulation in the adenylate cyclase-cyclic AMP system of rat liver.
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PMID:Sequential changes in hepatic polyamine, deoxyribonucleic acid, and cyclic adenosine 3',5'-monophosphate metabolism after subacute exposure to cadmium in rats. 19 91

A radioimmunoassay for cyclic AMP has been developed using protein A containing staphylococci as an immunoabsorbent. Protein A containing heat-killed staphylococci (Cowan I) are coated with rabbit antiserum raised against the 2'-O-succinyl derivative of cyclic AMP coupled to human serum albumin. After washing with a Tween 20 containing buffer, antibody coated staphylococci are diluted with heat-killed staphylococci devoid of protein A (staphylococcus epidermidis) and mixed with [125I]-2'-O-succinyl cyclic AMP tyrosine methyl ester, standards or unknowns. At the end of the incubation, separation of bound and free labelled antigen is achieved by bound and free labelled antigen is achieved by centrifugation. The results are comparable to those obtained with a precipitation assay using polyethylenglycol 6000. Acetylation prior to radioimmunoassay increases sensitivity about 80-fold. 50% depression of zero dose binding occurs at 15--16 femtomoles acetylated cyclic AMP. The crossreactivity with cyclic GMP, ATP, ADP, 5'-AMP and adenosine is extremely low. The present technique is an attractive alternative to the second antibody method or polyethylenglycol precipitation.
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PMID:Solid phase radioimmunoassay for cyclic AMP using staphylococcal protein A-antibody adsorbent. 19 25

Differences in sensitivity to catecholamines between colon and duodenum were examined in tissues from the rat, monitoring the depressive effect of catecholamines on contractile response to acetylcholine (ACh). The sensitivity of colonic tissue to ACh was higher than that of duodenal. Epinephrine (Ep, 10(-7) g/ml) depressed the contractile response to ACh in the colonic tissue, but not in the duodenal. The depressive effect of Ep on the contractile response to ACh is attributed to the stimulation of adrenergic beta-receptors in the colonic tissue as the depression disappeared by pretreatment with propranolol (10(-6) g/ml). There was no difference on the depressive effect of papaverine on the contractile response to ACh, except when low concentrations were used. Dibutyryl cyclic AMP (10(-4) g/ml) depressed the contractile responses of both tissues to ACh. After treatment with Ep (10(-7) g/ml), cyclic AMP content was increased in the colonic tissue but not in the duodenal. However, papaverine (3 X 10(-6 g/ml) and a higher dose of Ep(10(-6) g/ml) increased cyclic AMP content in both tissues. The increase of cyclic AMP and the decrease of tension caused by Ep were not correlated in these tissues. However, a positive correlation was observed between the depressive effect of Ep on the contractile response to ACh and the increase of cyclic AMP content in these tissues.
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PMID:Depressive effect of epinephrine mediated via adrenergic beta-receptor in isolated rat colon and duodenum. 19 72

ACTH, cholera toxin, cyclic AMP but not pregnenolone-induced steroidogenesis in Y-1 functional mouse adrenal tumor cells was significantly inhibited by delta-9-tetrahydrocannabinol, cannabidiol, and cannabinol. The inhibition of steroidogenesis could not be correlated with a general depression in cell function or viability. The data suggest that cannabinoids inhibit corticosteroidogenesis at a site between the synthesis of cAMP and of pregnenolone.
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PMID:Inhibition of cortiocosteroidogenesis by delta-9-tetrahydrocannabinol. 20 49

1 Following the observation that lymphocyte beta-adrenoceptor responsiveness was not depressed in asthmatics treated only with non-adrenergic drugs we have explored the effects of prolonged exposure to beta-adrenoceptor agonists in normal subjects. 2 Treatment with oral salbutamol (12-16 mg/kg/day for 10 days), or with inhaled salbutamol (3000 microgram/day for 8-10 days) resulted in a significant reduction in lymphocyte beta-adrenoceptor responsiveness. 3 A 48 h infusion of isoxsuprine (10 mg/h) resulted in a marked depression of lymphocyte beta-adrenoceptor responsiveness (P less than 0.001). 4 Prolonged elevation of endogenous catecholamines caused by phaeochromocytoma was also associated with a marked depression of lymphocyte beta-adrenoceptor responsiveness (P less than 0.001). 5 There was no evidence that an increase in phosphodiesterase activity could explain the reduced cyclic AMP response. 6 It is concluded that diminished beta-adrenoceptor response occurs as a response to prolonged exposure to beta-adrenoceptor agonists. It is likely that the diminished response seen in asthmatic subjects can be explained on a similar basis and does not indicate an inherent cellular defect. 7 The possible clinical significance of such changes in asthmatics are discussed.
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PMID:Desensitization of the beta-adrenoceptor of lymphocytes from normal subjects and patients with phaeochromocytoma: studies in vivo. 20 93

The acute in vitro action of adrenocorticotropin (ACTH) and corticosterone alone and in combination were determined in the Cloudman S-91 melanoma grown in vivo. Hormone-treated melanoma dice (5-240 min) were analyzed for tyrosinase activity (EC 1.14.18.1), cyclic AMP (cAMP) and cyclic GMP (cGMP). ACTH elevated cAMP levels in the S-91 melanoma. However, these increases in cAMP were not accompanied by increased tyrosinase activity. Corticosterone depressed cAMP levels while stimulating tyrosinase activity. ACTH plus corticosterone produced an early cAMP peak followed by depression. ACTH plus corticosterone stimulated tyrosine activity coincident with the early cAMP peak followed by a drop in tyrosinase activity which was subsequently elevated. cGMP levels were not altered by any hormone treatment. The results indicate that cAMP is not the sole modulator of tyrosinase activity and suggest the interaction of ACTH, corticosterone and cAMP in the regulation of melanoma tyrosinase activity.
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PMID:Glucocorticoid modulation of adrenocorticotropin-induced melanogenesis in the Cloudman S-91 melanoma in vitro. 20 85

The postulated disturbance of cyclic AMP (cAMP) in manic-depressive illness was investigated by using plasma as the biological material. Cyclic AMP was measured by a protein-binding assay, which was found very satisfactory for the purpose of this study. In the drug-free state, depressed patients (n = 28) had significantly lower and manic patients (n = 9) significantly higher plasma concentrations of cAMP than controls. Unmedicated manic-depressive subjects had normal cAMP levels during normothymic phases (n = 7). Cyclic AMP was reduced by neuroleptics in mania and elevated by tricyclics in depression. Lithium exerted a normalizing effect on cAMP in both phases of the illness. It is concluded that manic-depressive illness is associated with a disturbance in the cAMP system. The use of plasma rather than urine for the investigation of the state of cAMP in psychiatric disorders is advocated.
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PMID:Plasma cyclic AMP in manic-depressive illness. 20 68

The acute in vitro action of adrenocorticotropin (ACTH) and corticosterone alone and in combination were determined in the Harding-Passey (HP) melanoma grown in vivo. Hormone treated melanoma dice (5--240 min) were analyzed for tyrosinase activity, cyclic AMP (cAMP) and cyclic GMP (cGMP). ACTH elevated cAMP and cGMP levels 20- and 13-fold, respectively, in the HP melanoma. However, these large increases in cyclic nucleotide levels were accompanied by only a 49% increase in tyrosinase activity. Corticosterone elicited a similar response. ACTH plus corticosterone produced an early cAMP and cGMP peak followed by depression. ACTH plus corticosterone stimulated tyrosinase activity coincident with the early cyclic nucleotide peak followed by a drop in tyrosinase activity which was subsequently elevated. The results indicate that neither cAMP nor cGMP are the sole modulators of tyrosinase activity and suggest the interaction of ACTH, corticosterone and cyclic nucleotides in the regulation of melanoma tyrosinase activity.
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PMID:Interaction of ACTH, corticosterone and cyclic nucleotides in Harding-Passey melanoma melanogenesis. 21 Jul 23

1 Quantitative studies were made on the glucose release from rabbit liver slices in vitro induced by a range of concentrations of (-)-adrenaline (Ad), (-)-isoprenaline (Iso), glucagon and adenosine 3',5'-monophosphate (cyclic AMP) in the presence and absence of several concentrations of dihydroergotamine (DHE). 2 DHE (3.16 X 10(-6) M) shifted the Ad log concentration-response (LCR) curve to the right and also reduced the maximum response; at a higher concentration (3.16 x 10(-5) M) it produced a greater shift to the right of the LCR curve and caused a reduction in the slope and a larger depression of the maximal responses. The LCR curve to Iso was similarly affected by this higher concentration of DHE. 3 DHE (1 X 10(-5) M) produced no significant effect on the LCR curves of glucagon or cyclic AMP and even at 1 x 10(-4) M DHE caused only a slight depression of the maximal responses to both agonists without any modification of the lower major portions of the curves. 4 These data indicate a selective antagonism by DHE at the rabbit liver adrenoceptor and, since the maximal responses to catecholamines were depressed by a lower concentration of DHE than was required to produce a slight depression of the responses to glucagon and cyclic AMP, the antagonism of DHE against catecholamines does not appear to be at a site beyond the formation of cyclic AMP, but rather at a site more intimately related to the adrenoceptor.
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PMID:Differences in dihydroergotamine antagonism of glucose release by catecholamines, glucagon and adenosine 3',5'-monophosphate in rabbit liver slices. 21 Aug 74


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