Plasma Norepinephrine and Dopamine-β-Hydroxylase Activity in Schizophrenia

Castellani, Sam

doi:10.1001/archpsyc.1982.04290100021004

Cited by 47 publications

(11 citation statements)

References 51 publications

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“…Concerning basal blood pressure, previous results are contradictory. There are results in schizophrenics demon strating a lower blood pressure [9,[24][25][26], no difference [27][28][29][30][31], and elevated measures [32,33] in comparison to HV. However, especially for some studies showing lower levels, the influence of neuroleptic medication during the study period cannot be ruled out.…”

Section: Comparison With the Literature And Methodological Commentsmentioning

confidence: 99%

Orthostatic Challenge during Neuroleptic Test Dose: A Possible Predictor of Short-Term Outcome

Volz

Mackert²,

Diefenbacher³

et al. 1994

Neuropsychobiology

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Cardiovascular measurements were used as indicators of autonomic arousal during an orthostatic challenge test without medication and after a test dose of 150 mg perazine in 20 acute schizophrenic patients. Unmedicated schizophrenics showed elevated heart rates and elevated systolic and diastolic blood pressure in comparison to healthy volunteers. After a test dose of 150 mg perazine, responders (using BPRS outcome criteria after 23 days) showed a pronounced orthostatic heart rate reaction in comparison to nonresponders. Results are discussed in relation to arousal theories and central dopaminergic activity in schizophrenia.

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Section: Comparison With the Literature And Methodological Commentsmentioning

confidence: 99%

Orthostatic Challenge during Neuroleptic Test Dose: A Possible Predictor of Short-Term Outcome

Volz

Mackert²,

Diefenbacher³

et al. 1994

Neuropsychobiology

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“…Perhaps the most consistent observation in this regard is that patients who have unipolar major depression with psychotic features exhibit lower pD β H than depressed patients without such symptoms (Cubells et al 2002; Lykouras et al 1988; Meltzer et al 1976; Meyers et al 1999; Mod et al 1986; Sapru et al 1989): five studies have found such a relationship (Cubells et al 2002; Meltzer et al 1976; Meyers et al 1999; Mod et al 1986), and only one has not (Lykouras et al 1988). Studies of pD β H in schizophrenia clearly have ruled out a simple association between variation in pD β H and the diagnosis of the disorder, but some studies (Sternberg et al 1983; van Kammen et al 1994) have noted differences in symptomatic patterns, premorbid or morbid functioning, or in clinical course, associated with variation in pD β H activity, cerebrospinal fluid D β H activity, or protein levels [which are both highly correlated to pD β H (Castellani et al 1982; O'Connor et al 1994)]. The foregoing observations suggest that a detailed understanding of the genetics underlying pD β H might reveal important information about genetic modifiers of psychosis across a variety of psychiatric diagnoses.…”

Section: Introductionmentioning

confidence: 99%

Linkage analysis of plasma dopamine β-hydroxylase activity in families of patients with schizophrenia

Cubells

Sun

et al. 2011

Hum Genet

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Dopamine β-hydroxylase (DβH) catalyzes the conversion of dopamine to norepinephrine. DβH enters the plasma after vesicular release from sympathetic neurons and the adrenal medulla. Plasma DβH activity (pDβH) varies widely among individuals, and genetic inheritance regulates that variation. Linkage studies suggested strong linkage of pDβH to ABO on 9q34, and positive evidence for linkage to the complement fixation locus on 19p13.2-13.3. Subsequent association studies strongly supported DBH, which maps adjacent to ABO, as the locus regulating a large proportion of the heritable variation in pDβH. Prior studies have suggested that variation in pDβH, or genetic variants at DβH, associate with differences in expression of psychotic symptoms in patients with schizophrenia and other idiopathic or drug-induced brain disorders, suggesting that DBH might be a genetic modifier of psychotic symptoms. As a first step toward investigating that hypothesis, we performed linkage analysis on pDβH in patients with schizophrenia and their relatives. The results strongly confirm linkage of markers at DBH to pDβH under several models (maximum multipoint LOD score, 6.33), but find no evidence to support linkage anywhere on chromosome 19. Accounting for the contributions to the linkage signal of three SNPs at DBH, rs1611115, rs1611122, and rs6271 reduced but did not eliminate the linkage peak, whereas accounting for all SNPs near DBH eliminated the signal entirely. Analysis of markers genome-wide uncovered positive evidence for linkage between markers at chromosome 20p12 (multi-point LOD = 3.1 at 27.2 cM). The present results provide the first direct evidence for linkage between DBH and pDβH, suggest that rs1611115, rs1611122, rs6271 and additional unidentified variants at or near DBH contribute to the genetic regulation of pDβH, and suggest that a locus near 20p12 also influences pDβH.

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“…Treatment with haloperidol (3‐20 mg/day) for at least one year,30 or with haloperidol (5‐15 mg/day) for 3 weeks,31 does not alter plasma NE levels. On the other hand, treatment with chlorpromazine (400‐2,000 mg/day) for 8 days has been reported to raise levels of plasma NE 32. Comparative clinical studies of the effects of neuroleptics on plasma 3‐MT levels are scarce.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, treatment with chlorpromazine (400-2,000 mg/day) for 8 days has been reported to raise levels of plasma NE. 32 Comparative clinical studies of the effects of neuroleptics on plasma 3-MT levels are scarce. A preclinical study has reported that injection of haloperidol (0.5 mg/kg) or chlorpro-mazine (20 mg/kg) has no significant effect on brain 3-MT levels.…”

Section: Discussionmentioning

confidence: 99%

The Role of Noradrenergic and Dopaminergic Hyperactivity in the Development of Spontaneous Recurrence of Methamphetamine Psychosis and Susceptibility to Episode Recurrence

Yui

Gotō

Ikemoto

2004

Annals of the New York Academy of Sciences

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The role of dopaminergic activity in susceptibility of methamphetamine (MAP) psychosis (flashbacks) to subsequent spontaneous recurrences was studied. Plasma monoamine metabolite levels were assayed in 23 flashbackers, of whom 10 experienced a single flashback, 8 exhibited subsequent flashbacks and 5 with the last episode; 18 nonflashbackers with a history of MAP psychosis; 9 subjects with persistent MAP psychosis; and 19 MAP user and 10 nonuser controls. All flashbackers had undergone frightening stressful experiences during previous MAP use. Their flashbacks were triggered by mild psychosocial stressors. Plasma norepinephrine (NE) levels increased with the increase in plasma levels of 3-methoxytyramine (3-MT), an index of dopamine release, during flashbacks in the 23 flashbackers. Of these, the 8 with subsequent episodes had markedly increased NE levels and increased 3-methoxytyramine levels during flashbacks. However, the 5 flashbackers with the last episode had moderately increased NE levels, and the 10 with a single episode displayed small increases in NE levels during flashbacks. Their 3-MT levels did not significantly differ from the levels in the control groups. Thus, increased DA release in addition to robust noradrenergic hyperactivity in response to mild psychosocial stressors may be important in susceptibility to subsequent flashbacks.

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Plasma Norepinephrine and Dopamine-β-Hydroxylase Activity in Schizophrenia

Cited by 47 publications

References 51 publications

Orthostatic Challenge during Neuroleptic Test Dose: A Possible Predictor of Short-Term Outcome

Orthostatic Challenge during Neuroleptic Test Dose: A Possible Predictor of Short-Term Outcome

Linkage analysis of plasma dopamine β-hydroxylase activity in families of patients with schizophrenia

The Role of Noradrenergic and Dopaminergic Hyperactivity in the Development of Spontaneous Recurrence of Methamphetamine Psychosis and Susceptibility to Episode Recurrence

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