Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

33 cases of schizophrenia received normal food and no premedication. After a clinical improvement which showed itself 3--6 weeks after the beginning of the chlorpromazine treatment, the 17-ketosteroids, the 17-ketogenic steroids and also the electrolytes were dertermined in the blood serum, the erythrocytes and the urine. 12 schizophrenics each received 25 mg of ACTH for three days puring the maximum chlorpromazine dosage. The separate results of examination were tabulated. The final results showed a restriction in the steroid synthesis, an increase in the excretion of potassium through the kidneys along with a decrease in the excretion of sodium. There was an appreciable drop in the sodium potassium concentration in the erythrocytes. It can be assumed that there is a connection between the variations in the membrane permeability to electrolytes and pharmacogenic dyskinesia.
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PMID:The adrenocortical secretion in schizophrenics during chlorpromazine treatment. 20 56

Six cases of acute renal failure (ARF) due to rhabdomyolysis were experienced between 1984 and 1989. Patients' ages ranged from 33 to 92 years old (average ages 61) and all were male. The causes of rhabdomyolysis were as follows: one crush syndrome, one acute arterial occlusion, one diabetic hyperosmolar nonketotic coma and three cases of malignant syndrome due to neuroleptica (mainly haloperidol). Underlying diseases included, one case of abdominal aneurysm, two cases of diabetes mellitus, two cases of schizophrenia and one case of reactive psychosis. Dehydration was considered as an important factor in the onset of rhabdomyolysis and ARF, because it was observed in 4 of the cases in this study. In all cases, the serum levels of potassium, phosphorus and uric acid as well as myoglobin and myogenic enzymes increased markedly. In patients with myoglobinuric ARF, severe metabolic acidosis and hypocalcemia in the oliguric phase and hypercalcemia in the diuretic phase were prominent. Muscle biopsy showed myolytic degeneration in 2 of 4 cases. Five cases were treated with hemodialysis and one case was managed conservatively. All 6 cases had relatively good prognosis. However, 3 cases with malignant syndrome showed outcomes more severe than in the other 3 cases without such syndrome.
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PMID:[Acute renal failure due to rhabdomyolysis--clinical investigation on our 6 cases]. 163 34

Three mechanisms of lithium transport across erythrocyte membrane [lithium-sodium countertransport (LSC), lithium-potassium cotransport (LPC), and passive lithium diffusion (PLD)] were estimated in 27 acutely schizophrenic patients, 27 acutely depressed affective patients and in 18 control subjects. The activities of all mechanisms studied were significantly lower in both schizophrenic and depressed patients compared with controls. Analysis by gender showed that in control subjects, mean values of erythrocyte LSC and LPC were significantly higher in males compared with females. The decrease of LSC and LPC in depression and LSC in schizophrenia compared with control subjects was observed only in male patients but not in female ones. The results obtained suggest that lithium transport abnormalities during acute psychotic episodes are not specific to affective patients where lithium exerts its therapeutic action, but are also observed in schizophrenia. These abnormalities are more evident in male patients.
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PMID:Abnormalities of lithium transport across the erythrocyte membrane in depression and schizophrenia. 203 77

A case is presented of Torsade de Pointes (TDP) with T wave alternans in a 31-year-old female receiving a moderate dose of chlorpromazine. She was treated in an another hospital for schizophrenia with chlorpromazine (100 mg daily) for several years and admitted to Fujisawa city hospital for numerous episodes of syncope. The electrocardiogram immediately after admission revealed a marked QTc prolongation to 0.81 seconds, T wave alternation without any obvious change in morphology of the QRS complex, and recurrent ventricular tachycardia called TDP. The T wave alternans and TDP were easily abolished by intravenous administration of a bolus of 50 mg lidocaine infusion. The QT interval however, remained prolonged. Physical examination, including cardiac examination, was normal. Serum potassium was 3.6/mEq. Chlorpromazine was discontinued immediately after admission and no further episodes of TDP were seen after the first day. After the QT interval returned to almost normal, chlorpromazine (50 mg daily) was re-administered. Two days after the re-administration, the electrocardiogram revealed marked QT interval prolongation with prominent T waves. Psychotropic drugs, such as chlorpromazine, prolong the QT interval and cause TDP. Chlorpromazine appears to have been responsible for TDP and the T wave alternans in this case. TDP caused by a moderate dose of chlorpromazine has not been previously reported. Lone T wave alternans unaccompanied by changes in the QRS complex is a rare phenomenon and the mechanism underlying T wave alternans remains unknown.
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PMID:[Torsade de Pointes with T wave alternans in a patient receiving moderate dose of chlorpromazine: report of a case]. 221 93

The present review deals with the molecular mechanisms and elementary phenomena underlying the activation of the voltage- and chemo-sensitive membrane macromolecules: sodium- and potassium-ion channels and nicotinic ACh receptors and their associated ion channel. To achieve an understanding of their various kinetics and conformational states, a number of novel alkaloids, BTX, HTXs, gephyrotoxins, and certain psychotomimetic drugs such as phencyclidine, and many other pharmacologically active agents have been used. Biochemical assays and various electrophysiological techniques have been used in a number of biological preparations--e.g., Torpedo membranes, brain synaptosomes, amphibian and mammalian neuromuscular preparations--to describe the action of such agents. The availability of BTX and scorpion toxins together with aconitine and veratridine as activators and TTX and STX as antagonists of the voltage-sensitive sodium channels, made possible the identification and the physiological and pharmacological characterization of these channels. These studies provided the basis for understanding the mechanisms underlying electrical excitability and culminated, more recently, in the purification and reconstitution of sodium channels from rat brain and in the successful cloning of these channels with the elucidation of their primary structure. We now know that the sodium channel has a molecular mass of 316,000 daltons, consists of five subunits, and has multiple sites for various ligands. In contrast to sodium channels, various classes of potassium channels (inward and outward rectifier potassium channels and Ca(2+)-activated potassium channels) have been described. Unlike the sodium channels, there are no known specific activators for potassium channels. However, a number of potassium channel blockers such as 4-aminopyridine, HTX, histamine, and norepinephrine have been identified which complement the varying types of potassium channels in different neurons. One class of potassium channel blockers with profound medical and social implications comprises PCP and its analogues. The blockade of the potassium-induced 86Rb+ efflux from brain cells, the resulting prolongation of muscle and nerve action potentials, and the increase in transmitter release observed with PCP and some analogues are all highly suggestive of a role for the potassium channel in the behavioral effects of these drugs and its potential involvement in schizophrenia. A number of toxic principles of both plant and animal origin played a significant role in the development of our knowledge about the nAChR.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Macromolecular sites for specific neurotoxins and drugs on chemosensitive synapses and electrical excitation in biological membranes. 248 4

Data on an investigation and analysis of 8 cases taken neuroleptics followed by Adams-Stokes syndrome were reported. All patients were diagnosed as schizophrenia without cardiovascular diseases previously. In the process of treatment with 1 or 2 kinds of neuroleptics, Adams-Stokes syndrome appeared, while the potassium was in a range of 1.1--3.8 mEq/L. EKG profile varied, such as showed hypokalemia, ventricular flutter or fibrillation, frequent multifocal ventricular premature beat including bigeminy, and complained with second or third A-V block. The authors deem that neuroleptics may give rise to hypokalemia and then result in cardiac arrhythmias. Damage to heart tends to happen when more than one kind of neuroleptics were medicated. The treatment measures depend above all upon the active and effective attendance to hypokalemia. The patients may die from ventricular fibrillation without proper treatment.
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PMID:[Adams-stokes syndrome due to neuroleptic agents]. 257 65

The effect of zinc nutriture and metabolism on brain function has been reviewed. Zinc nutriture and its effect on the concentration and metabolism of essential elements (e.g. zinc, copper, manganese, magnesium, sodium, potassium and calcium) and on the concentration and metabolism of toxic elements (e.g. aluminum and lead) are discussed in relationship to brain function. In addition, possible interrelationships between zinc nutriture and metabolism and its effect on a number of diseases including acrodermatitis enteropathica, Pick's disease, Alzheimer's disease, schizophrenia, fifth day fits, and epilepsy are discussed. Descriptions and comparisons of methods to measure brain zinc are presented. Behavioral changes and the altered brain morphology which have been associated with zinc deficiency are reviewed. Some possible mechanisms for the association of anorexia with zinc deficiency are outlined. Perinatal brain damage produced by early zinc deficiency followed by rehabilitation with adequate zinc appears to be long term, maybe permanent. Interrelationships between zinc nutriture and aspects of neurochemistry are outlined. Some of the neurochemistries discussed include nucleic acid and protein synthesis, cytoskeletal proteins, neurotransmitters (e.g. catecholamines, indoleamines, glutamate, gamma-aminobutyric acid, and neuropeptides), neurotransmitter receptors, 7S nerve growth factor and zinc-binding proteins. Recent evidence linking zinc and neurotransmission is discussed.
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PMID:Zinc and the central nervous system. 330 3

Based on commonalities between peripheral blood "immunocytes" and central nervous system cells (both have receptors for endorphins, enkephalins, dopamine, acetylcholine, etc.) blocking of potassium ion channels in both brain cell synaptosome and suppressor T cells, and common sharing of antigenic determinants on one or another immunocyte and one or another CNS cells, we postulated that peripheral blood immunocytes can be used to study CNS mechanisms. In the present studies we used peripheral blood lymphocytes to study the effects of phencyclidine (PCP) on various receptors. This agent causes a permanent psychosis similar to chronic schizophrenia in a small percent of users. We observed similar effects in binding to sigma receptors, inhibition of binding and reversibility of binding in receptors of both human peripheral blood receptors and the mouse neuroblastoma, a hamster brain cell hybrid clone. The results are complete with the hypothesis that some cases of schizophrenia are immunologically mediated, perhaps due to antibodies to the sigma receptor. Alternatively, immunologic deficiency might hinder elimination of neurotropic viruses which in genetically predisposed individuals bind to and block the sigma receptor. Functional deficiency of the brain cell equivalent of lymphocyte suppressor T cells by one or another immunologic mechanisms or an excess of T helper cells might also cause schizophrenia by causing an excess of normal brain "B-cell equivalent cell" output response to sensory input.
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PMID:Sigma receptors and autoimmune mechanisms in schizophrenia: preliminary findings and hypotheses. 609 18

Antischizophrenic neuroleptic drugs of the diphenylbutylpiperidine class, which includes pimozide, fluspirilene, penfluridol, and clopimozide, inhibit [3H]nitrendipine binding with IC50 values of 13-30 nM. This inhibition involves receptors for the verapamil/prenylamine class of calcium channel antagonists. These diphenylbutylpiperidines also inhibit potassium-induced calcium-dependent contractions of rat vas deferens at concentrations of 40-350 nM. Other phenothiazine and butyrophenone neuroleptics lack such potent calcium-antagonist actions. Diphenylbutylpiperidines also differ from other neuroleptics in their ability to relieve negative symptoms of schizophrenia, such as emotional withdrawal, as well as the positive symptoms which respond to all neuroleptics. We suggest that these unique antischizophrenic actions are related to a blockade by diphenylbutylpiperidines of voltage-operated calcium channels.
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PMID:Antischizophrenic drugs of the diphenylbutylpiperidine type act as calcium channel antagonists. 613 40

sigma Receptors have been implicated in many pharmacological and physiological functions. sigma Receptors were purported to modulate behavioral alteration induced by cocaine and amphetamine, mediate effects of certain atypical antipsychotic agents, affect tonic potassium channels, the PCP/NMDA receptor complex, duodenal bicarbonate secretion, and CRF-induced colonic motility. sigma Receptors were reported to be altered in schizophrenia in certain studies, and up- and downregulations of sigma receptors have been observed in certain conditions. Neuropeptide Y has been shown to modulate the PCP/NMDA receptor complex in both central and gastrointestinal systems via sigma receptors. sigma Receptors are G-protein linked, and certain actions of sigma receptor ligands were affected by G-protein-modifying agents. Using photoaffinity labeling technique, a polypeptide of about 26 kDa has been identified as a sigma receptor. However, the exact biochemical relationship of this polypeptide to sigma receptors is unknown at present.
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PMID:Delineating biochemical and functional properties of sigma receptors: emerging concepts. 810 75


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