Urinary Cyclic AMP in ‘Endogenous' and ‘Neurotic’ Depression

1975 ◽  
Vol 126 (1) ◽  
pp. 49-55 ◽  
Author(s):  
K. Sinanan ◽  
A. M. B. Keatinge ◽  
P. G. S. Beckett ◽  
W. Clayton Love
Keyword(s):  
Cyclic Amp ◽  
Second Messenger ◽  
Adenyl Cyclase ◽  
Induced Responses ◽  
High Concentration ◽  
Cyclic Monophosphate ◽  
Cyclic Amp Phosphodiesterase ◽  
Urinary Cyclic Amp ◽  
The Brain

Since the discovery of adenosine 3'5'-cyclic monophosphate (cyclic AMP) by Sutherland and Rall (1958), the concept has evolved that this nucleotide acts as the second messenger substance for many neurotransmitter and hormone-induced responses (Sutherland, Robison and Butcher, 1968). Cyclic AMP occurs in high concentration in the brain. Cyclic AMP is functionally closely related, and possibly fundamental, to the action of catecholamines and serotonin, both of which have been implicated in the amine hypothesis of depression (Granville-Grossman, 1971). Cyclic AMP is formed from ATP by the action of an enzyme adenyl cyclase, and it is degraded by the enzyme cyclic-AMP-phosphodiesterase (Lancet, Editorial, 1970) both of which occur in brain.

The Effect of Mitomycin C on Platelet Aggregation and Adenosine 3′, 5′-Monophosphate Metabolism

1978 ◽  
Vol 39 (01) ◽  
pp. 177-185 ◽  
Author(s):  
Shuichi Hashimoto ◽  
Sachiko Shibata ◽  
Bonro Kobayashi
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Mitomycin C ◽  
Blood Platelets ◽  
Adenosine Diphosphate ◽  
Cellular Membrane ◽  
Adenyl Cyclase ◽  
Cyclic Amp Phosphodiesterase ◽  
Membrane Structure And Function ◽  
And Function

SummaryThe effect of Mitomycin C on aggregation, adenosine 3′, 5′-monophosphate (cyclic AMP) metabolism and reactions induced by thrombin was studied in rabbit platelets. Mitomycin C inhibited the platelet aggregation induced by adenosine diphosphate or thrombin. The level of radioactive cyclic AMP derived from 8-14C adenine or 8-14C adenosine increased after incubating intact platelets with Mitomycin G. Formation of radioactive adenosine triphosphate also increased though mitochondrial oxidation was not stimulated. Similar effect was observed also in rabbit liver. Mitomycin C failed to stimulate platelet adenyl cyclase but inhibited cyclic AMP phosphodiesterase in the absence of theophylline. In the platelets preincubated with Mitomycin C, thrombin-induced inhibition of adenyl cyclase, stimulation of membrane-bound cyclic AMP phosphodiesterase, and release of 250,000 dalton protein from platelet membranes were prevented. These results suggest that Mitomycin C will affect cellular membrane structure and function, and this extranuclear effect of Mitomycin C will lead to inhibition of aggregation in blood platelets.

Urinary Adenosine 3’,5′-Cyclic Monophosphate: Effects of Electroconvulsive Therapy

1976 ◽  
Vol 129 (2) ◽  
pp. 173-177 ◽  
Author(s):  
Richard B. Moyes ◽  
Isabel C. A. Moyes
Keyword(s):  
Cyclic Amp ◽  
Electroconvulsive Therapy ◽  
Consistent Pattern ◽  
Cyclic Monophosphate ◽  
Urinary Cyclic Amp

SummarySerial studies of urinary cyclic AMP in in-patients undergoing electroconvulsive therapy (ECT) have been carried out. No consistent pattern of change following ECT could be demonstrated. The results do not support earlier reports of large rises in urinary cAMP directly after administration of ECT.

Effect of Unconjugated and Conjugated Phenol and Uraemia on the Synthesis of Adenosine 3′:5′-Cyclic Monophosphate in Rat Brain Homogenates

1978 ◽  
Vol 55 (3) ◽  
pp. 271-275
Author(s):  
G. A. Turner ◽  
E. N. Wardle
Keyword(s):  
Rat Brain ◽  
Adenyl Cyclase ◽  
Cortical Response ◽  
Depressive Effect ◽  
Cyclic Monophosphate ◽  
Normal Rat ◽  
The Brain

1. The effects of phenol and phenyl glucuronide on the responses of normal rat brain adenyl cyclase to noradrenaline and dopamine have been investigated. Neurotransmitter responses have also been examined in brains from uraemic and normal rats. 2. A depressive effect of phenol on the adenosine 3′: 5′-cyclic monophosphate response of the neostriatum to dopamine was shown to be completely abolished if the toxin was present in the conjugated form; the response of the cortex to noradrenaline was stimulated by the presence of phenyl glucuronide, even though the unconjugated form had no effect. 3. The uraemic state in the rat also resulted in a depression of the neostriatum response to dopamine, yet an enhancement of the cortical response to noradrenaline. 4. The action of phenols on the brain is relevant to hepatic and uraemic coma.

BABIES, HORMONES AND KIDNEYS—A NEW LOOK AT DEVELOPMENT

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 3-4
Author(s):  
Wallace W. McCrory
Keyword(s):  
Cyclic Amp ◽  
Rat Kidney ◽  
Adenyl Cyclase ◽  
Endocrine Gland ◽  
Hormone Action ◽  
Abundant Evidence ◽  
Cell Target ◽  
Urinary Cyclic Amp ◽  
Adenyl Cyclase System

The role of cyclic AMP (adenosine 3’,5’-monophosphate) in hormone action is now quite firmly established. Abundant evidence now demonstrates that after release from an endocrine gland a hormone (first messenger) is transported to its effector cell (target) where it interacts with the adenyl cyclase system to release cyclic AMP (second messenger) which acts intracellularly to carry out the work of the hormone. In 1967, Chase and Aurbach demonstrated that urinary cyclic AMP, now known to be derived from both plasma and kidney, increased when parathormone (PTH) was administered to the rat and man. These workers also demonstrated a PTH-sensitive adenyl cyclase in the proximal tubules of the rat kidney and in fetal bone.

STUDIES ON THE MECHANISMS OF SOMATOSTATIN ACTION ON INSULIN RELEASE

1977 ◽  
Vol 85 (2) ◽  
pp. 379-388 ◽  
Author(s):  
A Claro ◽  
V. Grill ◽  
S. Efendić ◽  
R. Luft
Keyword(s):  
Cyclic Amp ◽  
Insulin Release ◽  
Competitive Inhibition ◽  
Phosphodiesterase Inhibitor ◽  
Adenyl Cyclase ◽  
Phosphodiesterase Activity ◽  
High Concentration ◽  
Isolated Islets Of Langerhans ◽  
Cyclic Amp Accumulation ◽  
Effect Of Glucose

ABSTRACT The effects of somatostatin on insulin release and cyclic AMP metabolism were studied in collagenase-isolated islets of Langerhans from the rat. Concentrations from 500 to 2000 ng/ml significantly inhibited glucose stimulated insulin release, while 100 and 200 ng/ml were ineffective. Somatostatin (2000 ng/ml) inhibited insulin release and [3H]-cyclic AMP accumulation induced by 16.7 mm glucose after 10 and 30 min of incubation. In dose-response studies, the inhibition by somatostatin of the effect of glucose on [3H] cyclic AMP and insulin release could be overcome by a high concentration of the hexose (44.9 mM), suggesting competitive inhibition. In the absence of glucose, somatostatin inhibited [3H] cyclic AMP accumulation induced by the phosphodiesterase inhibitor, IBMX, while no inhibition was seen, again in the absence of hexose, when the [3H] cyclic AMP levels had been raised by the adenyl cyclase stimulator, cholera toxin. Somatostatin did not affect phosphodiesterase activity when added to islet homogenates, but preincubation of the islets with the peptide before homogenization decreased the activity by about 30 %. It is suggested that somatostatin-induced inhibition of insulin release is, at least partially, mediated by cyclic AMP, probably through an action on islet adenyl cyclase.

Inhibition of cAMP Phosphodiesterase by Some Phototherapeutic Agents

1987 ◽  
Vol 42 (7-8) ◽  
pp. 1009-1010 ◽  
Author(s):  
Lucia Bovalini ◽  
Paola Lusini ◽  
Sandra Simoni ◽  
Daniela Vedaldi ◽  
Lucio Andreassi ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Puva Therapy ◽  
High Concentration ◽  
Camp Phosphodiesterase ◽  
Cyclic Amp Phosphodiesterase ◽  
Significant Inhibitory Effect ◽  
Light Inhibition

The behaviour of cyclic-3′,5′-AMP phosphodiesterase has been studied in the presence of psoralen, 8-methoxy-psoralen (8-MOP), 4,5′,8-trimethylpsoralen (TMP) (usu­ ally used in PUVA therapy), 4.6,4′-trimethylangelicin (TMA) and khellin recently proposed for the same thera­ peutical use. TMP and TMA exhibit a significant inhibitory effect on cyclic AMP phosphodiesterase; a light inhibition is produced by khellin at rather high concentration.

Urinary Excretion of Adenosine 3’: 5′-Cyclic Monophosphate in Depressive Illness

1974 ◽  
Vol 125 (586) ◽  
pp. 275-279 ◽  
Author(s):  
Graham J. Naylor ◽  
David A. Stansfield ◽  
Susan F. Whyte ◽  
Frederick Hutchinson
Keyword(s):  
Cyclic Amp ◽  
Urinary Excretion ◽  
Affective State ◽  
Depressive Illness ◽  
Control Group ◽  
Cyclic Monophosphate ◽  
Manic Depressive ◽  
Two Samples ◽  
Urinary Cyclic Amp ◽  
Depressive Patients

Changes in the excretion of adenosine 3’:5′-cyclic monophosphate (cyclic AMP) have been reported in depressive illness. Abdulla and Hamadah (1970) reported that urinary cyclic AMP excretion was lower than normal during depression and increased with recovery. However, these results were based on single 24-hour urine collections during depression and on recovery, with no creatinine estimations to suggest that the collections were complete. There was no control of diet, drugs or activity. The controls do not appear to have been matched for age. Paul, Ditzion, Pauk and Janowsky (1970) reported that the cyclic AMP excretion in neurotic depression was higher and in psychotic depression was lower than in a control group, but neither difference was statistically significant. However, on enlarging the study by including more psychotic depressives they reported that the cyclic AMP excretion of this group was significantly less than that of the controls (Paul, Cramer and Goodwin, 1971). These workers had controlled the patients' drug and dietary (but not fluid) intake. There appeared to be only minimal control of activity. The results were based on approximately two samples of urine per subject, which were very carefully checked for completeness of collection. Unfortunately the age of the controls (19–22 years) was very different from that of the patients (25–64 years). On two small groups of patients treated with either Laevodopa or lithium carbonate, they reported that changes in affective state were accompanied by changes in the urinary excretion of cyclic AMP. However, in serial studies on manic-depressive patients Paul, Cramer and Bunney (1971) failed to show a correlation between mood rating and cyclic AMP excretion in five out of seven patients; but they reported that the cyclic AMP excretion was increased on the day of rapid switch from depression to mania. The above groups of workers had used an enzymatic-isotope displacement technique to estimate the cyclic AMP. Brown, Salway, Albano, Hullin and Ekins (1972), using a saturation method to assay cyclic AMP, found no correlation between mood and cyclic AMP excretion in two short-cycle manic-depressive patients. Jenner, Sampson, Thompson, Somerville, Beard and Smith (1972) wrote: ‘We have measured daily excretion by a number of depressed and manic depressive patients over periods covering several mood changes without being able to establish any consistent correlation between cyclic AMP excretion and mood, … However, in one unusual case we have found a very marked correlation‘. We (Naylor, Dick, Dick, Moody and Stansfield, 1974) were unable to demonstrate any relationship between urinary cyclic AMP excretion and mood in a patient with recurrent psychotic episodes, in which depressive features predominated.

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