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)

Recent experimental data are summarized about changes in the functioning of calcium ion channels in clonal cellular lines (pheochromocytoma PC12) and hippocampal neurons of newborn rats on the background of altered intracellular level of aromatic amino acid L-tyrosine or its precursors L-phenylalanine. Elevation of the level of L-phenylalanine persistently down-regulated the high-threshold voltage-operated calcium channels in both types of cells without affecting the low-threshold ones in hippocampal neurons. This depression could be to some extent reversed by elevation of the level of L-tyrosine. Thus both amino acids seem to exert a long-lasting antagonistic modulatory effect on the corresponding channels, mediated probably through changes in tyrosylation of some cytoskeletal proteins. The participation of these molecular mechanisms in brain dysfunction during congenital disease phenylketonuria is suggested.
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PMID:[Possible molecular mechanisms of brain dysfunction in phenylketonuria]. 130

Lithium salts are considered the most effective agents used in treating manic-depression. Previous studies in PC12 pheochromocytoma cells indicate that lithium has a dramatic augmenting effect on expression of the fos proto-oncogene, a component of the AP-1 transcription factor. Although fos expression is activated by agonists that function through different signal transduction pathways, the lithium augmenting effect appears to be specific for receptor and post-receptor stimulators of protein kinase C (PKC). In particular, fos induction mediated by the m1 muscarinic receptor linked to PKC activation was found to be exquisitely sensitive to lithium enhancement. We now show that a similar augmenting effect can be demonstrated in rat brain. Following treatment with the muscarinic agonist pilocarpine, fos mRNA accumulates in the cortex, an effect that is blocked by the m1 antagonist pirenzepine. Rats treated with a single intraperitoneal injection of lithium chloride exhibited a substantial increase in pilocarpine-mediated fos expression. In contrast, fos expression induced in several brain regions by a single electroconvulsive shock is not augmented by lithium. The finding that short-term treatment with lithium enhances fos expression in the brain suggests a mechanism for its therapeutic action.
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PMID:Lithium augments pilocarpine-induced fos gene expression in rat brain. 171 37

Pheochromocytomas can mimic many unrelated diseases due to their various presenting signs; they are encountered very rarely in childhood. Recently, their neuropsychiatric aspects have become a subject of interest for many workers, but most of the findings reported previously have been observed in adults. We present a case report which is unique in that it concerns a child with pheochromocytoma and psychiatric findings consisting of depression and panic disorder, which were interpreted as being directly related to, since they disappeared after the removal of, the tumor. Depression was persistent and accompanied by a constricting-type headache, while panic disorder was acute and accompanied by a migraine-type headache. Another intriguing complication encountered in our case was jaundice; we considered that it could possibly have been due to an adverse effect of catecholamines on hepatocyte function. We conclude that a pheochromocytoma can be confused with neuropsychiatric disorders in children as well as in adults and that it should be considered in the differential diagnosis of such disorders.
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PMID:Pheochromocytoma presenting with headache, panic attacks and jaundice in a child. 177 65

A 59 year-old housewife was admitted to the emergency service with a sudden onset of chest pain and nausea. Initially she was treated as an acute myocardial infarction, but conventional treatments were not effective, and she was sent to our hospital for further evaluation. Her ECG showed several abnormal findings including T-wave inversion, atrial flutter, QT-time prolongation, ST-segment depression or elevation, and frequent ventricular ectopic beats. The echocardiogram, 201thallium scintigram and coronary angiography were almost normal. Both urinary and plasma levels of catecholamines were remarkably increased, and the plasma epinephrine was extremely high during attacks. Abdominal echotomography and CT-scanning showed a large left adrenal tumor. The 131MIBG scintiscan revealed a high accumulation in this tumor. Then the patient was diagnosed as having pheochromocytoma and catecholamine-induced myocarditis. The administration of phentolamine (10 mg) normalized the inversion of T-wave and the high blood pressure. But when propranolol (2 mg) was administrated in addition to phentolamine, the ECG showed a biphasic low T-wave change. According to these phenomena, we supposed that the alpha-adrenergic receptor was involved in the development of the ST-T changes of the ECG, and the alpha-adrenergic receptor of this patient might be sensitive under excessive catecholamines, according to the inhibition of the beta-receptor by propranolol.
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PMID:[A case of pheochromocytoma with an AMI-like ECG change corrected by an alpha-blocking agent]. 196 1

This study tests the hypothesis that atrial natriuretic factor (ANF) and C-ANF(4-23)-NH2 (C-ANF) augment cGMP generation and inhibit both cAMP generation and depolarization-induced catecholamine release in nerve growth factor treated pheochromocytoma cells by a pertussis toxin (PTX)-sensitive mechanism. Synthetic rat ANF(99-126) and the clearance receptor antagonist C-ANF (10(-12)-10(-9) M) inhibited basal and 5 microM vasoactive intestinal peptide (VIP)-induced cAMP generation in a concentration-dependent manner. These actions of ANF and C-ANF were blocked by 12-18 h pretreatment with PTX (100 ng/ml), suggesting ANF receptor coupling to adenylate cyclase via an inhibitory guanine nucleotide-binding protein. Both ANF (10(-11)-10(-9) M) and C-ANF (10(-11)-10(-8) M) also inhibited K(+)-induced catecholamine release in a concentration-dependent manner. ANF (10(-11)-10(-8) M) increased cGMP generation in a concentration-dependent manner but C-ANF did not. The accumulation of cGMP in response to ANF was not altered by treatment with PTX. Therefore, PTX dissociated the increased concentrations of cGMP from the ANF-mediated depression of evoked catecholamine release. C-ANF also dissociated elevations in cGMP concentrations from an ANF-mediated attenuation of evoked catecholamine release. The results of this study indicate that ANF inhibits adrenergic neurotransmission independent of guanylate cyclase.
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PMID:Neuromodulatory effects of atrial natriuretic factor are independent of guanylate cyclase in adrenergic neuronal pheochromocytoma cells. 197 29

A forty-two-year-old man was admitted because of chest pain. Electrocardiograms at admission showed horizontal ST depression in leads, II, III, aVF, V4, V5, and V6. Direct blood pressure monitoring revealed cyclic change between 160/100 mmHg and 70/50 mmHg and heart rate between 80/sec and 120/sec at fifteen minute intervals. The plasma norepinephrine and epinephrine concentrations were elevated during the episodes of hypertension. Pheochromocytoma was found in the right adrenal gland. These cyclic changes in blood pressure and heart rate are an aid for diagnosis.
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PMID:Pheochromocytoma with electrocardiographic change mimicking angina pectoris, and cyclic change in direct arterial pressure--a case report. 200 62

The authors studied 8 patients (4 males and 4 females) with Cushing's syndrome due to ectopic ACTH secretion. Chronological age ranged from 15 to 45 years and duration of the disease ranged from 3 to 48 months. All patients presented typical signs of Cushing's syndrome, blood hypertension, and four of them had hyperpigmentation of the skin. Five patients had fasting hyperglycemia and all patients but one had serum hypokalemia (serum K = 2.2 to 3.9mEq/l). The circadian rhythm of cortisol was absent in all patients and basal cortisol levels were elevated in all patients but one. Basal ACTH levels evaluated in 7 patients were elevated in 6 (29 to 1050 pg/ml-MRC). One patient presented normal depression of urinary 17-OH after two days of dexamethasone and normal increase of urinary 17-OH and serum 11-dexycortisol after methyrapone. Four patients had carcinoid tumor (3 thymic and 1 bronchial), two had pancreatic islets cell tumors, one had bilateral pheochromocytoma and medular carcinoma of the thyroid, and one had oat cell carcinoma of the lung and medular carcinoma of the thyroid. Thoracic X-rays identified the ectopic ACTH secretion tumor in four cases, all confirmed by CT scan. Abdominal CT showed a difuse enlargement of the adrenals in seven cases and bilateral nodules in one case (pheochromocytomas). Six patients died within 3 years of the diagnosis. The authors concluded that clinical and hormonal findings could mislead the findings of ACTH ectopic secretion and Cushing's disease, and suggest that thoracic X-rays and CT scans of the skull, thorax, and abdome should be done in all cases of Cushing's syndrome.
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PMID:[Cushing syndrome due to ectopic ACTH secretion]. 255 51

It is known that nerve growth factor (NGF) induces neurite outgrowth and elevation of the activity of adrenergic marker enzyme, tyrosine hydroxylase (TH) in clonal rat pheochromocytoma cells (PC12), whereas glioma-conditioned medium (GCM) induces neurite outgrowth and elevation of the activity of cholinergic marker enzyme, choline acetyltransferase (ChAT) in PC12 cells. In the previous study we have shown that retinoic acid (RA) induces specific elevation of ChAT activity and depression of TH activity without morphological differentiation (Matsuoka, I. et al., Brain Res., 502 (1989]. In the present study, we compared the effects of NGF, GCM and RA on the intracellular signalings in PC12 cells in relation to the mechanism of cholinergic differentiation. Addition of NGF, GCM or RA to the culture medium of PC12 cells caused a rapid rise in intracellular Ca2+ concentration [( Ca2+]i) reaching the level of almost 2.5-fold the resting condition within 3-18 h. Thereafter, [Ca2+]i of NGF-treated cells were decreased to the resting level within 12 h. On the other hand, [Ca2+]i of GCM-and RA-treated cells decreased to a level which was 1.8- to 2-fold the resting condition within 24-48 h and stayed at this level for up to 4-7 days. When homogenates of GCM- and RA-treated PC12 cells were incubated with [gamma-32P]ATP, phosphorylation of a protein with molecular mass of 27 kDa (27 K-protein) was specifically enhanced. The phosphorylation of the 27 K-protein was not seen in the homogenate of the NGF-treated cells. The phosphorylation of the 27 K-protein was dependent on Ca2+ and inhibited by inhibitors of Ca2+-dependent protein kinase, H-7 and W-7. Addition of H-7 and W-7 to the culture medium of PC12 cells abolished the elevation of ChAT activity specifically induced by GCM and RA. These observations suggested that the sustained increase of [Ca2+]i and Ca2+-dependent protein phosphorylation are involved in the intracellular signaling mechanism required for the cholinergic differentiation of PC12 cells induced by GCM and RA.
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PMID:Possible involvements of intracellular Ca2+ and Ca2+ -dependent protein phosphorylation in cholinergic differentiation of clonal rat pheochromocytoma cells (PC12) induced by glioma-conditioned medium and retinoic acid. 258

During infection with herpes simplex virus type 1 (HSV-1) the activity of tyrosine hydroxylase (TH) in PC12 pheochromocytoma cells was initially depressed reaching a nadir at 6 hours post-inoculation, but recovered rapidly with a return to baseline activity by 8 to 9 hours post-inoculation. Subsequently, TH activity again fell with a second more variable rise in activity occurring at 24 hours post-inoculation. Studies with metabolic inhibitors and 2 temperature-sensitive viral mutants indicated that these alterations of TH activity were dissociated from morphological cytopathology and likely required expression of "late" viral gene products. Immunotitration using anti-TH antibody suggested that early depression of TH activity resulted principally from loss of enzyme protein rather than simple enzyme inactivation, and that reconstitution of activity at 9 hours was related to augmented enzyme synthesis. These observations illustrate the complexity of perturbed cellular metabolism during HSV-1 infection and suggest involvement of two unexpected processes: alteration of a specialized cell function as a result of viral genes expressed late in the replicative cycle, and augmented synthesis of a cell-coded gene product during the course of infection.
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PMID:Alteration of tyrosine hydroxylase activity in PC12 cells infected with herpes simplex virus type 1. 285 60

We have studied the changes in the levels of the enzyme molecule and mRNA for poly(ADP-ribose) synthetase during nerve growth factor-promoted neurite outgrowth in rat pheochromocytoma PC12 cells. When the PC12 cells were cultured in the presence of nerve growth factor, the content of enzyme molecules decreased along with neurite outgrowth to 50% of the original amounts in 2 days and the content of mRNA for the enzyme also decreased to approximately 50% in 2 days. These results suggest that the decrease of the enzyme molecule may be due to depression of expression of the gene for synthetase during the process. Taken together with previous observations, the decrease of the synthetase seems to be required for some cellular differentiation.
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PMID:Decrease in the level of poly(ADP-ribose) synthetase during nerve growth factor-promoted neurite outgrowth in rat pheochromocytoma PC12 cells. 313 66


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