Urinary Excretion of Cyclic Amp and Manic-Depressive Psychosis

1972 ◽  
Vol 120 (557) ◽  
pp. 405-408 ◽  
Author(s):  
B. L. Brown ◽  
J. G. Salway ◽  
J. D. M. Albano ◽  
R. P. Hullin ◽  
R. P. Ekins
Keyword(s):  
Cyclic Amp ◽  
Urinary Excretion ◽  
Affective Disorders ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Subjects ◽  
Manic Depressive Psychosis ◽  
Manic Depressive ◽  
Mental Symptoms ◽  
Manic Patients

Recently several communications have been published implicating impaired 3′5′ cyclic adenosine monophosphate (cyclic AMP) metabolism as a causal factor in affective disorders (1, 3, 7, 8, 9, 11). In particular, the urinary excretion of cyclic AMP in manic patients is reported to be increased compared with that of normal subjects, whereas in depressed patients a decreased excretion has been observed (1, 7, 8, 9). These findings form the basis of a theory explaining the systemic and mental symptoms of affective disorders (1).

Manic-Depressive Psychosis and Urinary Excretion of Cyclic AMP

1972 ◽  
Vol 121 (561) ◽  
pp. 236-237 ◽  
Author(s):  
F. A. Jenner ◽  
Gwyneth A. Sampson ◽  
Elizabeth A. Thompson ◽  
A. R. Somerville ◽  
Nicol A. Beard ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Urinary Excretion ◽  
Manic Depressive Psychosis ◽  
Manic Depressive

scholarly journals SITE OF ACTION OF 3',5'-CYCLIC ADENOSINE MONOPHOSPHATE IN PRODUCTION OF TRYPTOPHANASE IN ESCHERICHIA COLI

Genetics ◽  
1972 ◽  
Vol 70 (1) ◽  
pp. 175-180
Author(s):  
LaDonna Immken ◽  
David Apirion
Keyword(s):  
Escherichia Coli ◽  
Cyclic Amp ◽  
Messenger Rna ◽  
Rna Synthesis ◽  
Polypeptide Chain ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Chain Elongation ◽  
Site Of Action

ABSTRACT 3″,5″ cyclic-AMP (cAMP) will stimulate the rate of tryptophanase synthesis in Escherichia coli cultures induced with tryptophan. Adding cAMP after the initiation of messenger RNA synthesis was blocked by rifampicin, did not stimulate tryptophanase synthesis. This indicates that cAMP acts at initiation of either transcription or translation and not at the level of chain elongation of either the messenger or the polypeptide chain.

scholarly journals Cyclic AMP response element-binding protein is required in excitatory neurons in the forebrain to sustain wakefulness

SLEEP ◽  
2020 ◽  
Author(s):  
Mathieu E Wimmer ◽  
Rosa Cui ◽  
Jennifer M Blackwell ◽  
Ted Abel
Keyword(s):  
Cyclic Amp ◽  
Intracellular Signaling ◽  
Target Genes ◽  
Binding Protein ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Response Element ◽  
Creb Phosphorylation ◽  
Element Binding Protein ◽  
And Control

Abstract The molecular and intracellular signaling processes that control sleep and wake states remain largely unknown. A consistent observation is that the cyclic adenosine monophosphate (AMP) response element-binding protein (CREB), an activity-dependent transcription factor, is differentially activated during sleep and wakefulness. CREB is phosphorylated by the cyclic AMP/protein kinase A (cAMP/PKA) signaling pathway as well as other kinases, and phosphorylated CREB promotes the transcription of target genes. Genetic studies in flies and mice suggest that CREB signaling influences sleep/wake states by promoting and stabilizing wakefulness. However, it remains unclear where in the brain CREB is required to drive wakefulness. In rats, CREB phosphorylation increases in the cerebral cortex during wakefulness and decreases during sleep, but it is not known if this change is functionally relevant to the maintenance of wakefulness. Here, we used the Cre/lox system to conditionally delete CREB in the forebrain (FB) and in the locus coeruleus (LC), two regions known to be important for the production of arousal and wakefulness. We used polysomnography to measure sleep/wake levels and sleep architecture in conditional CREB mutant mice and control littermates. We found that FB-specific deletion of CREB decreased wakefulness and increased non-rapid eye movement sleep. Mice lacking CREB in the FB were unable to sustain normal periods of wakefulness. On the other hand, deletion of CREB from LC neurons did not change sleep/wake levels or sleep/wake architecture. Taken together, these results suggest that CREB is required in neurons within the FB but not in the LC to promote and stabilize wakefulness.

Lithium administration and phosphate excretion

1976 ◽  
Vol 231 (4) ◽  
pp. 1140-1146 ◽  
Author(s):  
JA Arruda ◽  
JM Richardson ◽  
JA Wolfson ◽  
L Nascimento ◽  
DR Rademacher ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Renal Cortex ◽  
Cyclic Adenosine Monophosphate ◽  
Fractional Excretion ◽  
Adenosine Monophosphate ◽  
Adenyl Cyclase ◽  
Phosphate Excretion ◽  
Camp System

The phosphaturic effect of parathyroid hormone (PTH), cyclic adenosine monophosphate (cAMP), acetazolamide (Az), and HCO3 loading was studied in normal, thyroparathyroidectomized (TPTX), and Li-treated dogs. PTH administration to normal animals markedly increased fractional excretion (F) of PO4 but had a blunted effect on FPO4 in the Li-treated animals. Cyclic AMP likewise markedly increased FPO4 in the normal animals but had a markedly blunted effect in the Li-treated animals. Az led to a significant increase in FNa, FHCO3, and FPO4 in the normal animals. In the Li-treated dogs, Az induced a significant natriuresis and bicarbonaturia but failed to increase phosphaturia. HCO3 loading in normal dogs caused a significant phosphaturia while having little effect on FPO4 in Li-treated dogs. HCO3 loading to TPTX dogs was associated with a lower FPO4 as compared to normal HCO3-loaded animals. These data suggest that Li administration not only blocks the adenyl cyclase-cAMP system in the renal cortex, but it may also interfere with a step distal to the formation of cAMP, since the phosphaturic effect of both PTH and cAMP was markedly diminished in Li-treated animals.

Family Psychiatric Morbidity, Parental Deprivation and Socio-Economic Status in Cases of Mania

1975 ◽  
Vol 126 (2) ◽  
pp. 191-192 ◽  
Author(s):  
H. D. Chopra
Keyword(s):  
Affective Disorder ◽  
Psychiatric Illness ◽  
Economic Status ◽  
Psychiatric Morbidity ◽  
Parental Death ◽  
Manic Depressive Psychosis ◽  
Socio Economic Status ◽  
First Degree Relatives ◽  
Manic Depressive ◽  
Manic Patients

Manic-depressive psychosis is considered to comprise two different clinical entities, bipolar and monopolar. This dichotomy is based mainly on Western clinical material. The present study aimed at eliciting any differences that might exist between monopolar and bipolar manic patients in respect of three factors: (i) occurrence of psychiatric illness in first degree relatives; (ii) parental death before the patient's 15th birthday; and (iii) socio-economic status of the patient. Venkoba Rao (1973) studied the differences between monopolar and bipolar endogenous depressives on three factors: occurrence of affective disorder (including suicide) in first degree relatives; parental loss before the patient's 12th birthday, and the extent of ‘jointness' of the patient's family.

Lithium and erythrocyte membrane cation carrier studies in normal and manic depressive subjects

1977 ◽  
Vol 7 (2) ◽  
pp. 229-233 ◽  
Author(s):  
G. J. Naylor ◽  
A. Smith ◽  
L. J. Boardman ◽  
D. A. T. Dick ◽  
E. G. Dick ◽  
...  
Keyword(s):  
Erythrocyte Membrane ◽  
Human Subjects ◽  
Normal Subjects ◽  
Sodium Concentration ◽  
Manic Depressive Psychosis ◽  
Manic Depressive ◽  
Normal Human ◽  
Potassium Influx ◽  
Erythrocyte Sodium

synopsisChanges in the erythrocyte membrane cation carrier following lithium ingestion in normal human subjects were studied; ouabain sensitive potassium influx fell significantly during the lithium treated phase. Lithium was fed to rats and no change in erythrocyte Na-K ATPase was shown. These findings contrast with studies of lithium in manic depressive psychosis. The fluctuations in the erythrocyte membrane cation carrier were studied in 5 normal subjects over 12 weeks and the correlations between the parameters calculated. The erythrocyte sodium concentration correlated positively with the ouabain sensitive potassium influx. This too contrasts with findings in manic depressive psychosis.

DIFFERENT EFFECTS OF EXOGENOUS CYCLIC ADENOSINE MONOPHOSPHATE AND ITS DIBUTYRYL DERIVATIVE ON PLASMA GROWTH HORMONE, GLUCOSE, INSULIN AND CORTISOL

1976 ◽  
Vol 83 (1) ◽  
pp. 15-25
Author(s):  
M. Vanderschueren-Lodeweyckx ◽  
W. Proesmans ◽  
E. Eggermont ◽  
R. Eeckels
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Subjects ◽  
Immunoreactive Insulin ◽  
Plasma Growth Hormone ◽  
Hormone Levels ◽  
The Mean

ABSTRACT The effects of the infusion in four different dosages (0.001, 0.005, 0.02 and 0.2 mg/kg/min during 60 min) of cyclic 3′,5′-adenosine monophosphate and of its dibutyryl derivative on plasma growth hormone and on glucose, immunoreactive insulin and cortisol were studied in 38 normal subjects and in 10 patients with idiopathic hypopituitarism. In normal subjects cyclic 3′,5′-adenosine monophosphate provokes an increase in plasma growth hormone levels (only when a dosage of 0.2 mg/kg/min is used) without any changes in plasma glucose, insulin and cortisol. The maximal value of the means is observed 75 min after starting the infusion. Dibutyryl cyclic 3′,5′-adenosine monophosphate (0.2 and 0.02 mg/kg/min) provokes a dose-related rise in plasma growth hormone levels which is always preceded by hyperglycaemia and hyperinsulinaemia. The peak of the mean growth hormone levels occurs at 135 min after initiation of the infusion. In all but one hypopituitary patients the nucleotides do not promote growth hormone secretion. It is concluded that exogenous cyclic 3′,5′-adenosine monophosphate and its dibutyryl derivative may not be considered as analogous and that both compounds may contribute to study growth hormone release in normal subjects and in patients with growth abnormalities.

scholarly journals IMMUNOLOGICAL RELEASE OF HISTAMINE AND SLOW REACTING SUBSTANCE OF ANAPHYLAXIS FROM HUMAN LUNG

1972 ◽  
Vol 136 (3) ◽  
pp. 556-567 ◽  
Author(s):  
Michael Kaliner ◽  
Robert P. Orange ◽  
K. Frank Austen
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Human Lung ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Target Cells ◽  
Human Lung Tissue ◽  
Adrenergic Agents ◽  
Protein Assay

The immunologic release of histamine and slow reacting substance of anaphylaxis (SRS-A) from human lung tissue can be enhanced by stimulation with either alpha adrenergic agents (phenylephrine or norepinephrine in the presence of propranolol) or cholinergic agents (acetylcholine or Carbachol). The finding that atropine prevents cholinergic but not comparable alpha adrenergic enhancement is consistent with the view that cholinergic and alpha adrenergic agonists interact with separate receptor sites on the target cells involved in the immunologic release of chemical mediators. The consistent qualitative relationship between the antigen-induced release of mediators and the level of cyclic adenosine monophosphate (cyclic AMP) as measured by the isolation of 14C-labeled cyclic AMP after incorporation of adenine-14C into the tissues or by the cyclic AMP binding protein assay suggests that changes in the level of this cyclic nucleotide mediate adrenergic modulation of the release of histamine and SRS-A. The addition of 8-bromo-cyclic guanosine monophosphate (cyclic GMP) produces an enhancement of the immunologic release of mediators while dibutyryl cyclic AMP is inhibitory. As cholinergic-induced enhancement was not associated with a measurable change in the levels of cyclic AMP, the possibility is suggested that cyclic GMP may be the intracellular mediator of cholinergic-induced enhancement of the immunologic release of histamine and SRS-A.

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