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)

The proceedings of the inaugural scientific meeting of the Society for Research on Nicotine and Tobacco (SRNT) are summarized. The primary objective of the meeting was to foster the exchange of information on the effects of nicotine and tobacco use, as well as factors which influence their use, drawing from biological, behavioral and social sciences. Much of this research can be viewed as a tale of "two" drugs--nicotine as a key to an important public health problem, and nicotine as a classical tool of physiological and pharmacological research. A historical overview of research on "both" drugs is provided first. Public policy alternatives for reducing the prevalence of tobacco use have been derived in part from basic and clinical research results and are briefly outlined. Evidence for genetic determinants on nicotine use and effects is presented using data from twin studies and from molecular genetic research with humans and animals. Consistent with this research, there is evidence of individual differences in pharmacokinetics and effects of nicotine, which could account for differences in smoking behavior and nicotine dependence. Finally, recent developments in the therapeutic uses of nicotine and novel nicotinic agonists with schizophrenia, Alzheimer's disease, Parkinson's disease, Tourette's syndrome and ulcerative colitis are presented. Overall, the research presented at the meeting demonstrated the vast diversity of areas of study involving nicotine and tobacco, as well as the rich opportunities for cross-communication among researchers from different disciplines.
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PMID:Society for Research on Nicotine and Tobacco. 882 21

Nine monoamine receptor antagonists have been compared for their potency to inhibit both spontaneously occurring and DOI ((1-)2,5-dimethoxy-4-iodophenyl)-2-aminopropane)-induced head-shakes (HS). Ritanserin, ketanserin, prazosin, haloperidol, pimozide, SCH 23390 and SCH 39166 potently and dose-dependently antagonised both types of HS while sulpiride and raclopride produced weak and partial antagonism. The potency of these agents to inhibit spontaneous HS and DOI-induced HS was closely correlated (r = 0.94) and was significantly related to 5HT2A receptor and to alpha 1-adrenoceptor affinities taken from published sources. Potency was independent of affinity for D2 receptors but there was a possible influence of D1 receptor affinity. HS have been proposed to model Tourette's Syndrome; thus the present findings may have implications for the mechanism of action of antipsychotic agents in this condition and possibly also in schizophrenia. Contrary to previous suggestions, 5HT2A receptors may be tonically activated under physiological conditions.
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PMID:Similarities in the pharmacology of spontaneous and DOI-induced head-shakes suggest 5HT2A receptors are active under physiological conditions. 895 81

The role of calcium in the etiology of anxiety has been proposed for several decades. Calcium channel blockers profoundly influence calcium metabolism and the transport of calcium. Even though the evidence for the role of calcium remains weak, drugs affecting calcium might be useful in the treatment of anxiety disorders. One of these compounds, verapamil, has been used to treat mood disorders. Calcium channel blockers have also been tried in other indications such as premenstrual syndrome, irritable bowel syndrome, schizophrenia, tardive dyskinesia, and Tourette's syndrome. However, the number of articles on the use of calcium channel blockers in the treatment of anxiety disorders is low. Three reports (two open, one double-blind) described some success in the treatment of panic disorder with verapamil, diltiazem, or nimodipine and one open-label study described unsuccessful treatment of anxiety and phobia with nifedipine in patients with various anxiety disorders. Further double-blind placebo-controlled studies of calcium channel blockers in the treatment of anxiety disorders are warranted to determine a possible role of these compounds in the armamentarium of antianxiety drugs.
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PMID:Calcium channel blockers for anxiety disorders? 898 18

This study was designed to validate an in vivo measurement of the functional sensitivity of basal ganglia neuronal circuits containing dopamine D2 receptors. We hypothesized that a D2 agonist would decrease striatopallidal neuronal activity, and hence regional cerebral blood flow (rCBF) over the axon terminals in the globus pallidus. Quantitative pallidal blood flow was measured using positron emission tomography (PET) with bolus injections of H215O and arterial sampling in six baboons before and after intravenous administration of the selective D2 agonist U91356a. We also tested whether the response to U91356a was modified by previous acute administration of various antagonists. Another baboon had serial measurements of blood flow under identical conditions, but received no dopaminergic drugs. In all animals that received U91356a, pallidal flow decreased in a dose-related manner. Global CBF had a similar response, but the decline in pallidal flow was greater in magnitude and remained significant after accounting for the global effect. A D2 antagonist, but not antagonists of D1, serotonin-2, or peripheral D2 receptors, prevented this decrease. This work demonstrates and validates an in vivo measure of the sensitivity of D2-mediated basal ganglia pathways. It also supports the hypothesis that activation of the indirect striatopallidal pathway, previously demonstrated using nonselective D2-like agonists, can be mediated specifically by D2 receptors. We speculate that the U91356a-PET technique may prove useful in detecting functional abnormalities of D2-mediated dopaminergic function in diseases such as parkinsonism, dystonia, Tourette syndrome, or schizophrenia.
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PMID:PET measurement of dopamine D2 receptor-mediated changes in striatopallidal function. 909 51

We present a unique case of an 18-year-old male who had a classic picture of schizophrenia preceded by a well documented history of Tourette Disorder and a developmental disorder. The subject, a member of an ongoing study on first-admission psychosis, has been systematically evaluated and followed up for two years, and the interesting neuropsychological findings are presented and compared to those of the rest of the sample with a diagnosis of schizophrenia. The triad of schizophrenia, Tourette Disorder and developmental disorder is described for the first time in a subject with an adult type schizophrenia. Possible neurodevelopmental impairments explaining the clinical picture are discussed in view of the recent literature.
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PMID:Developmental disorder, Tourette disorder and schizophrenia: a case study. 933 30

Nicotinic acetylcholine receptors are allosteric ligand-gated ion channels present in muscle and brain. Recent studies suggest that mutations altering their functional properties may produce congenital myasthenia and familial frontal lobe epilepsy. Current research also indicates that although nicotinic ligands often possess addictive properties, they could serve as therapeutic agents for Alzheimer's disease and Tourette's syndrome, as well as for schizophrenia.
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PMID:Pathological mutations of nicotinic receptors and nicotine-based therapies for brain disorders. 938 54

Abnormal sensory inhibition is a measurable indicator of a sensory processing deficit which is observed in schizophrenia, and other disorders, and which may be heritable. This deficit has also been observed in certain inbred mouse strains where the intensity of the deficit has been correlated with reduction in the number of hippocampal alpha-bungarotoxin-sensitive nicotinic receptors. Nicotine and certain nicotinic agonists produce brief periods of normal sensory inhibition in these mice. Similarly, nicotine also transiently normalizes sensory inhibition in schizophrenics. The present study assessed the effects of a novel nicotinic partial agonist (GTS-21), selective for the alpha-bungarotoxin site, on sensory inhibition in DBA mice, a strain with no sensory inhibition under routine experimental conditions. GTS-21 produced a dose-dependent normalization of sensory inhibition which was blocked by alpha-bungarotoxin but not mecamylamine. In contrast to other nicotinic agonists, normalization of sensory inhibition by GTS-21 and two related anabaseine compounds, DMAB-anabaseine and DMAC-anabaseine, was observed when administered a second time to the animal, after a 40-min delay. Our results indicated that the anabaseine compounds increase sensory inhibition through alpha7 nicotinic receptors, and that their ability to act repeatedly on these receptors may be less affected by desensitization.
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PMID:Selective alpha7-nicotinic agonists normalize inhibition of auditory response in DBA mice. 960 May 76

The D3-dopamine receptor gene, DRD3, has been considered as a candidate gene in several disorders in which the dopaminergic system has been implicated including Tourette syndrome and schizophrenia. The DRD3 studies to date have all used as the gene marker a Bal I polymerase chain reaction restriction fragment length polymorphism (PCR RFLP). There have been recent reports on a second marker, an Msp I PCR RFLP, that lies 40 kb downstream. We have typed a sample of 16 Tourette syndrome families with both markers and observed significant linkage disequilibrium between the two markers but no apparent association of either marker with Tourette syndrome.
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PMID:The Bal I and Msp I polymorphisms in the dopamine D3 receptor gene display, linkage disequilibrium with each other but no association with Tourette syndrome. 968 22

Nicotinic acetylcholine receptors are ligand-gated ion channels present in muscle and brain. These allosteric oligomers may exist in several conformational states which include a resting state, an open-channel state, and a desensitized refractory state. Recent work has shown that point mutations in the nicotinic receptor may, altogether, abolish desensitization, increase apparent affinity for agonists and convert the effect of a competitive antagonist into an agonist response. These pleiotropic effects are interpreted in terms of the allosteric model. This paper reviews recent evidence that such mutations occur spontaneously in humans and may cause diseases such as congenital myasthenia or familial frontal lobe epilepsy. In addition, nicotinic receptors are involved in tobacco smoking. Accumulating evidence, including experiments with knock-out animals, indicates that addiction to nicotine is linked to the activation of beta 2-subunit containing nicotinic receptors in the dopaminergic mesolimbic neurons which are part of the reward systems in the brain. Current research also indicates that nicotinic agonists might serve as therapeutic agents for Alzheimer's disease and Tourette's syndrome, as well as for schizophrenia. This paper extends and updates a recently published review.
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PMID:Allosteric nicotinic receptors, human pathologies. 978 46

Key substantive findings from quantitative and molecular genetic research are reviewed in relation to affective disorder, schizophrenia, autism, hyperkinetic/attention deficit disorder, oppositional and conduct disorders, drug/alcohol problems, and Tourette's syndrome/chronic tics.
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PMID:Genetics and child psychiatry: II Empirical research findings. 1010 25


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