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)

Yohimbine, an alpha 2-adrenergic receptor antagonist that increases noradrenergic function, was administered to 16 healthy subjects and 18 drug-free schizophrenic patients with (n = 10) and without (n = 8) tardive dyskinesia (TD). Outcome measures of this double-blind, placebo-controlled study included changes in behavior, plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG) level, blood pressure, and heart rate. A subgroup of six patients experienced a notable dysphoric arousal reaction that occurred 60 to 90 minutes following administration of 20 mg of yohimbine, this reaction was not observed in healthy subjects. The schizophrenic group as a whole (not the subgroup) showed a statistical trend toward a greater yohimbine-induced increase in plasma MHPG level and systolic sitting blood pressure. The patients with TD did not differ from those without TD or from healthy controls in their response to yohimbine. These results do not support the hypothesis that noradrenergic dysfunction plays a strong central role in the pathogenesis of schizophrenia or TD. However, further studies of noradrenergic dysfunction in sub-groups of patients with schizophrenia are indicated.
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PMID:Noradrenergic function in schizophrenia. 366 45

A study on the biology of 'panic disorder,' which I have classified under the category of 'anxiety disorder,' made progress recently. In a genetic study, the hereditary of panic disorder was checked by a 'linkage and twins' study, and the anticipation of panic disorder was recognized as being the same as that which is also found in the psychiatric conditions known as schizophrenia and manic depression. A panic disorder patient regards the anxious sign of a model as ruinous, and this weakness in recognition has been duly noted. Therefore, I studied a patient showing a continuance state of 'hyper-sensitivity,' and compared this to a patient showing a 'sleep disorder.' Noradrenaline plays an important role in anxiety as suppression of the locus ceruleus (LN), the major NE-containing nucleus of the noradrenaline nervous system, brings on a calming effect. Yohimbine, however, which is an alpha 2 antagonist, is found to induce panic attacks. The fact that selective serotonin reuptake inhibitor (SSRI) suppresses panic attacks suggests that serotonin is connected with panic disorders. It is also thought that the 'raphe nucleus' is the site of origin of the serotonin nervous system, which participates in the control of anxiety. This suggests the participation of a gamma-aminobutyric acid (GABA) nervous system in which the administration of benzodiazepine at a high potency would be an effective agent against panic disorder. Cholecystokinin (CCK) is also suggested to have a connection with panic disorder as CCK-4 causes panic attacks. There has been no CCK antagonist found effective for an object- or time-oriented panic disorder at the present. It is thought that corticotropin-releasing factor (CRF) is released during a panic attack. The development of a new CRF receptor antagonist is needed. In addition to the studies on the neurotransmitters of the traditional type, such as noradrenaline, serotonin and GABA, studies on the neuropeptides, such as CCK and CRF have become important for future consideration. Understanding this, image studies such as MRI, SPECT, fMRI and PET have become highly desirable.
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PMID:[Neuropharmacological and genetic study of panic disorder]. 1049 83

The noradrenergic system may play a role in antipsychotic modulation of schizophrenia symptoms. Therefore, the antagonistic potencies of the antipsychotics clozapine, chlorpromazine, risperidone, olanzapine, haloperidol, quetiapine, ziprasidone, iloperidone and aripiprazole were quantified using cell lines expressing the recombinant human alpha(2C)-adrenoceptor, alpha(2A)-adrenoceptor, or dopamine D(2L) receptor. The alpha(2)-adrenoceptor antagonists, yohimbine and idazoxan, were also tested. Alterations in cAMP were measured as changes in luminescence. In the alpha(2A)-adrenoceptor cell line, the agonist 5-bromo-6-(2-imidazolin-2-ylamino)quinoxaline (UK14,304) induced a concentration-dependent increase in luminescence. In cell lines expressing alpha(2C) and D(2L) receptors, agonists induced a concentration-dependent reduction in luminescence. Yohimbine and idazoxan were the most potent alpha(2A)-adrenoceptor antagonists, yohimbine and iloperidone were the most potent alpha(2C)-adrenoceptor antagonists, and haloperidol and olanzapine were the most potent dopamine D(2) receptor antagonists. Clozapine had the highest alpha(2C)/D(2) selectivity, and iloperidone the highest alpha(2C)/alpha(2A) ratio. It is hypothesised that alpha(2C)-adrenoceptor blockade contributes to improvement of cognitive function.
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PMID:alpha2C-Adrenoceptor blockade by clozapine and other antipsychotic drugs. 1259 Oct 93