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)

Biological tests may help clarify the relationship of schizoaffective disorder to major depressive disorder (MDD) and schizophrenia (SCZ). Thyrotropin-releasing hormone (TRH), 500 micrograms, was administered intravenously to eight schizoaffective depressed (SD), ten SCZ, 23 MDD patients and 43 healthy controls (HC), all males, ages 20-66 years and drug-free. Research Diagnostic Criteria (RDC) were utilized for establishing diagnoses, Hamilton Rating Scale for Depression (HRSD) total scores were used for assessing depressive symptoms. There were no differences in dmax PRL (post-TRH prolactin peak minus baseline, mean +/- SD) amongst SD, SCZ and HC groups (27.3 +/- 5.2, 28.8 +/- 5.4 and 31.5 +/- 5.6 ng/ml respectively). Mean dmax PRL in MDD was significantly lower than each of the other three groups (17.1 +/- 2.2 ng/ml, P less than 0.05 for all). The essentially normal PRL response to TRH in SD, significantly different from MDD but similar to SCZ parallels our previous observations on the pattern of thyrotropin (TSH) response to TRH in the same diagnostic groups. These biological findings may be taken to indicate that schizoaffective disorder, depressed subtype, is closer to schizophrenia than to major depressive disorder. However, they cannot be considered definitive evidence to that effect since schizoaffective disorders are known to be quite heterogeneous, and since the utilized biological tests lack specificity.
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PMID:Prolactin response to thyrotropin-releasing hormone in schizoaffective depressed compared to depressed and schizophrenic men and healthy controls. 212 54

The cause of the amenorrhea that occurs in patients with hyperprolactinemia is unknown. The involvement of endogenous opioid peptides in the inhibition of GnRH release as a central factor leading to the hypogonadotropic state has been recently described. This study analyzed the LH response to opiate receptor blockade by naloxone (4 mg, iv) in groups of subjects with amenorrhea due to hyperprolactinemia of different etiologies. Patients presenting with a PRL-secreting pituitary adenoma (n = 7), idiopathic hyperprolactinemia (n = 9), or hyperprolactinemia during pharmacological treatment for schizophrenia (n = 5) were studied. Furthermore, to evaluate whether high circulating PRL levels influence the activity of the opioid system after the menopause, a group of seven postmenopausal subjects was tested before and 1 week after the administration of metoclopramide (10 mg, three times a day), a dopamine receptor antagonist. Normal premenopausal women (n = 6) served as controls. Naloxone significantly increased plasma LH levels in both prolactinoma and idiopathic hyperprolactinemic patients (P less than 0.01 vs. basal and placebo). In neither of those groups was a significant correlation found between the plasma LH response to naloxone and basal plasma PRL levels. In contrast to pathological hyperprolactinemia, blockade of opiate receptors did not significantly change LH secretion in either amenorrheic women with pharmacologically induced hyperprolactinemia or postmenopausal women. These results suggest that the effect of hyperprolactinemia on opioid modulation of LH secretion is related to the nature of the hyperprolactinemic state, supporting the existence of increased opioid inhibition of LH levels in pathological hyperprolactinemia.
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PMID:Differences in the opioid control of luteinizing hormone secretion between pathological and iatrogenic hyperprolactinemic states. 288 Aug 62

Male patients suffering from borderline personality disorder (n = 13), major depression (n = 13) or schizophrenia (n = 13) were investigated on several psychopathological (HDRS, BPRS) and neuroendocrinological (DST and TSH, PRL, GH responses to TRH) parameters. Comparisons were made between the borderline group and the other groups of patients. Borderline patients differed from schizophrenics psychopathologically (BPRS) and neuroendocrinologically (DST). Also, borderline patients differed from major depressives in the HDRS, but behaved like them concerning DST. Our findings support the hypothesis that there are neuroendocrinological similarities between borderline personality disorder and major depressive patients, especially on the hypothalamo-pituitary-adrenal axis.
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PMID:Multiple neuroendocrinological responses in borderline personality disorder patients. 312 3

We studied the non-specific responses of GH and PRL to gonadotropin releasing hormone (GnRH) in eleven male patients aged 18-30 in whom a diagnosis of acute schizophrenia was made according to Crow's criteria. GnRH administration was followed by a significant increase in plasma GH in five patients; plasma PRL increased in two patients. The two prolactin responders were also GH responders. Non-specific GH response was confirmed on repeated testing in two patients in whom GnRH stimulation was performed twice. During saline control, non-specific hormone responses were not observed. The abnormal hormone responses observed in acute schizophrenia are probably due to the disordered monoamine regulation characteristic of this condition.
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PMID:Gonadotropin releasing hormone elicits abnormal hormone responses in schizophrenia. 391 Dec 48

Hypothalamo-pituitary functions were examined in thirteen children with behavioral disorders (six with hyperkinesia, four with autism, two with tic and one with schizophrenia) before and during treatment with pimozide, an antidopaminergic drug. The mean (+/- S.E.M.) basal serum PRL level (24.5 +/- 4.2 ng/ml) during pimozide treatment was significantly higher than that (12.4 +/- 3.2 ng/ml) before treatment. Hyperresponse of PRL to TSH releasing hormone (TRH) was observed in five (three with hyperkinesia, one with tic and one with autism) of the thirteen patients before treatment and in seven (four with hyperkinesia, two with autism and one with tic) during treatment. Mean TSH response during treatment was not significantly different from that before treatment. However, three of the four autistic children showed hyperresponse of TSH to TRH before treatment, whereas only one also showed a hyperresponse during treatment. The pimozide treatment had no demonstrable influence on GH or cortisol secretion in response to insulin-induced hypoglycemia, or on serum T4 and T3 levels.
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PMID:Influence of pimozide on hypothalamo-pituitary function in children with behavioral disorders. 642 90

To evaluate hypothalamic-pituitary-gonadal axis in acute schizophrenia, plasma FSH and LH concentrations were estimated both in basal conditions and after stimulation with gonadotropin releasing hormone (GnRH, 200 micrograms i.v.) in 14 young male patients with acute schizophrenia and in a age-matched group of 14 healthy male controls. Basal plasma PRL and testosterone levels were also measured. The mean basal levels of LH and FSH were slightly lower in schizophrenics, while the mean testosterone and prolactin levels were similar in the two groups. The FSH response to GnRH was significantly reduced in patients with acute schizophrenia, while the response of LH was similar in schizophrenics and in the controls. The possible significance of these findings is discussed in the contest of the complex neuroendocrine regulation of gonadotropin secretion and the overactivity of dopaminergic systems in acute schizophrenia.
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PMID:Gonadotropin response to gonadotropin releasing hormone in acute schizophrenia. 643 79

LH, FSH, PRL and testosterone were estimated by radioimmunoassay in serial venous samples from 20 male chronic schizophrenic patients, 17 age-matched controls, 3 patients in remission from acute schizophrenia, and in single samples from age-sex matched populations. LH and FSH, but not testosterone or PRL, were significantly reduced in patients with chronic schizophrenia. There was an associated reduction in the frequency, but not amplitude, of LH secretory episodes in patients with chronic schizophrenia. No abnormalities of LH secretion were detected in those patients in remission from acute schizophrenia. Fourteen of the chronic schizophrenic patients were retested at a later date with similar results, except in the case of the few patients who had been started on neuroleptic medication. Some relationships were established between hormonal secretion and the clinical features of these patients. The possible significance of these findings is discussed in the context of the complex control of gonadotropin secretion from the anterior pituitary and the natural history and nature of chronic schizophrenia.
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PMID:Gonadotropin secretion abnormalities in chronic schizophrenia. 680 36

Dopamine is a small and relatively simple molecule that fulfills diverse functions. Within the brain, it acts as a classical neurotransmitter whose attenuation or overactivity can result in disorders such as Parkinson's disease and schizophrenia. Major advances in the cloning and characterization of biosynthetic enzymes, transporters, and receptors have increased our knowledge regarding the metabolism, release, reuptake, and mechanism of action of dopamine. Dopamine reaches the pituitary via hypophysial portal blood from several hypothalamic nerve tracts that are regulated by PRL itself, estrogens, and several neuropeptides and neurotransmitters. Dopamine binds to type-2 dopamine receptors that are functionally linked to membrane channels and G proteins and suppresses the high intrinsic secretory activity of the pituitary lactotrophs. In addition to inhibiting PRL release by controlling calcium fluxes, dopamine activates several interacting intracellular signaling pathways and suppresses PRL gene expression and lactotroph proliferation. Thus, PRL homeostasis should be viewed in the context of a fine balance between the action of dopamine as an inhibitor and the many hypothalamic, systemic, and local factors acting as stimulators, none of which has yet emerged as a primary PRL releasing factor. The generation of transgenic animals with overexpressed or mutated genes expanded our understanding of dopamine-PRL interactions and the physiological consequences of their perturbations. PRL release in humans, which differs in many respects from that in laboratory animals, is affected by several drugs used in clinical practice. Hyperprolactinemia is a major neuroendocrine-related cause of reproductive disturbances in both men and women. The treatment of hyperprolactinemia has greatly benefited from the generation of progressively more effective and selective dopaminergic drugs.
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PMID:Dopamine as a prolactin (PRL) inhibitor. 1173 29

The aim of the research was to select some easily available and easily replicable biological markers that could be used as predictors of both acute and long-term therapy. A selection of state markers (structural computer tomography [CT] parameters, psychological parameters, tests concentrating on attention and memory, "soft signs"), trait markers (quantified electroencephalograph [QEEG], cortisolemia, prolactinemia [PRL], and their changes) and clinical symptoms (Positive and Negative Syndrome Scale [PANSS], Clinical Global Impression [CGI]) were determined in 52 hospitalised schizophrenic patients showing either an acute episode or an exacerbation. The evaluation was repeated after one year of outpatient therapy. The parameters studied so far are not sufficiently specific and sensitive; therefore, the prediction cannot be based on a single parameter. In order to overcome this shortcoming, we carried out the analysis by means of multidimensional statistics, applying discriminant analysis. The results of both a broader and a more specific approach are stated in the paper. In all the used examples of discriminant analysis, the optimum discriminator is cortisolemia or its changes after administering dexamethasone and structural CT parameters. The results indicate that combinations of vulnerability markers and state markers (cortisolemia) may be of predictive value and are compatible with the vulnerability-stress ethiopathogenetic model of schizophrenia.
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PMID:Biological markers and possibilities for predicting therapeutic results in schizophrenia: a methodological contribution. 1218

Recent studies have shown that medial prefrontal cortex (mPFC) lesions impair performance on a number of rodent tests of attention. Although this evidence clearly suggests a role for the rat mPFC in attentional functions, it is unclear whether subcortical changes associated with mPFC lesions might also be relevant to the neuropsychological deficits observed. Given the ample evidence suggesting increased dopaminergic mechanisms in the basal ganglia following mPFC lesions, we investigated the effects of dopamine receptor agonists and antagonists on the attentional deficits associated with mPFC lesions. Rats trained on a five-choice reaction time task received either complete mPFC lesions or lesions restricted to its ventral subregions, the prelimbic and infralimbic cortices (PRL-IL). Compared with sham-operated rats, animals in both the lesioned groups were impaired at responding correctly to the visual targets, although this deficit was more marked in mPFC-lesioned rats. In addition, both lesions were associated with increased perseverative responding. The accuracy deficits of rats with mPFC lesions were alleviated by systemic administration of the dopamine D2 receptor antagonist sulpiride. In contrast, rats with PRL-IL damage were not affected and control rats were impaired by sulpiride. Administration of either the dopamine D1 receptor antagonist SCH 23390 or of pre-synaptic doses of apomorphine had similar, albeit non-significant effects. Higher doses of any of these drugs non-specifically impaired performance. These results extend previous findings of attentional impairments in rats with mPFC lesions and are compatible with recent hypotheses concerning the role of dopaminergic dysregulation in the pathogenesis of schizophrenia.
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PMID:Sulpiride alleviates the attentional impairments of rats with medial prefrontal cortex lesions. 1249 30


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