Relationship Between Central and Peripheral Serotonin Indexes in Depressed and Suicidal Psychiatric Inpatients

Mann, J. John; McBride, Paul; Brown, Ryan P.; Linnoila, Markku; Leon, Andrew C.; DeMeo, Michael; Mieczkowski, Tom; Myers, Joyce E.; Stanley, Michael

doi:10.1001/archpsyc.1992.01820060022003

Cited by 259 publications

(152 citation statements)

References 19 publications

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“…The cur rent study suggests that prolactin response to fenflura mine challenge should be positively correlated with CSF-S-HlAA concentrations, which has recently been demonstrated in human beings (Mann et al 1992). et al 1988).…”

Section: Discussionmentioning

confidence: 69%

Low Versus High Prolactin Responders to Fenfluramine Challenge: Marker of Behavioral Differences in Adult Male Cynomolgus Macaques

Botchin

Kaplan

Manuck

et al. 1993

Neuropsychopharmacol

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Prolactin response to acute administration of fenfluramine hydrochloride is considered an indirect assessment of "net" central serotonergic activity. This study compared behavioral characteristics of adult, male cynomolgus macaques (Macaca fascicularis) having "low" or "high" prolactin responses to fenfluramine challenge. The subjects were 75 animals housed in five-member social groups for 28 months. In month 23, prolactin responses to fenfiuramine challenge were evaluated. Obseroations of specific behaviors (aggressive, submissive, affiliative, and nonsocial) were made three times per week on animals in eIlch social group. The dominance status of each animal within a social group was assessed at weekly illtervals.Low prolactin respOllders had a significantly higher index KEY WORDS: Aggression; Serotonin; Fenfluramine; Prolactin; Cynomolgus macaques; Social behaviorStudies in human beings demonstrate a relationship between low serotonergic activity and the propensity for impulsive aggression among violent criminal offend-

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Section: Discussionmentioning

confidence: 69%

Low Versus High Prolactin Responders to Fenfluramine Challenge: Marker of Behavioral Differences in Adult Male Cynomolgus Macaques

Botchin

Kaplan

Manuck

et al. 1993

Neuropsychopharmacol

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“…Notably, the association with schizophrenia seems stronger in Caucasians (Abdolmaleky et al, 2004). Another limitation is that the peripheral 5-HT 2A platelet binding is not a direct measure of the brain 5-HT 2A binding, and different transcription factors may regulate the gene in neurons expressing HTR 2A gene centrally compared with megakaryocytes (Mann et al, 1992;Pandey et al, 1995). The nonassociation of this genotype with binding in the depressed population may reflect other regulatory effects, associated with diagnosis, that need to be identified.…”

Section: Limitationsmentioning

confidence: 99%

Association of Serotonin 5-HT2A Receptor Binding and the T102C Polymorphism in Depressed and Healthy Caucasian Subjects

Khait

Huang

Zalsman

et al. 2004

Neuropsychopharmacol

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Serotonin 5-HT 2A receptor (5-HT 2A ) binding is reported to be altered in individuals with suicidal behavior, mood disorders, and aggressive-impulsive traits. Genetic association with major depression, suicidal behavior, and aggressive-impulsive traits has not been established. This study examines the possible association of the 5-HT 2A gene C102T polymorphism with the receptor binding kinetics, and clinical overt phenotypes. The study population included 63 healthy volunteers and 152 subjects with mood disorders, 56 of whom had a history of suicide attempts. All were Caucasian. Platelet 5-HT 2A binding kinetics (B max and K D ) were assayed and adjusted for seasonal variation. All subjects were genotyped for the T102C polymorphism. Clinical phenotype was determined by structured clinical interview. The TT genotype was associated with higher B max in all subjects (F ¼ 3.53, df ¼ 2,211; p ¼ 0.03), controlling for diagnosis. Bonferroni-adjusted post hoc testing showed higher binding in the TT compared with TC genotype in the control group (F ¼ 7.56, df ¼ 2,60, p ¼ 0.001), but not in the mood-disordered subjects. No difference was found in genotype and allele distribution between the mood-disordered subjects, with and without suicide attempt history, and controls. B max was not related to a diagnosis of mood disorders.The TT genotype appears associated with higher platelet 5-HT 2A B max in the healthy population, but this genotypic effect appears absent in mood disorders and unrelated to psychopathology.

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“…We have hypothesized that there is a serotonergic abnormality contributing to the diathesis or vulnerability for suicidal acts (Mann 1998). Lower levels of CSF 5-HIAA (Åsberg et al 1986b) and a blunted prolactin response to fenfluramine (Mann et al 1992) correlate with the presence and lethality of past suicide attempts in patients with major depression and can predict future suicide or suicide attempts (Roy et al 1989;Träskman-Bendz et al 1992;Nordström et al 1994). The association between suicide attempts and low CSF 5-HIAA has also been reported in schizophrenia and personality disorders, indicating that this association is independent of diagnosis.…”

mentioning

confidence: 99%

“…See Table 1 for a summary (Malone and Mann 1993;Owens and Nemeroff 1994;Stoff and Mann 1997;Mann 1998). In major depression there are fewer platelet serotonin transporters (5-HTT), lower CSF 5-HIAA (Mendels et al 1972;Sjöström and Roos 1972;Ashcroft et al 1973aAshcroft et al , 1973bPost and Goodwin 1974;Bowers 1974;Goodwin and Post 1977;van Praag and de Haan 1979;Koslow et al 1983;Åsberg et al 1984;Gerner et al 1984;Roy et al 1985;Redmond et al 1986), as well as a reduced growth hormone (GH) response to 5-hydroxytryptophan (5-HTP) (Upadhyaya et al 1991) and a blunted prolactin (PRL) response to oral fenfluramine (Siever et al 1984;Coccaro et al 1989;O'Keane and Dinan 1991;Mann et al 1992) and to intravenous L-tryptophan (Heninger et al 1984;Cowen et al 1990;Price et al 1991;Upadhyaya et al 1991). The antidepressant efficacy of selective serotonin reuptake inhibitors (SSRIs) suggests the abnormality in depression probably includes impaired serotonergic function, because selective enhancement of serotonergic activity is therapeutic (Åsberg et al 1986a).…”

mentioning

confidence: 99%

The Neurobiology and Genetics of Suicide and Attempted Suicide: A Focus on the Serotonergic System

Mann

2001

Neuropsychopharmacology

358

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Neuro-receptors Major depression and suicidal behavior are independently related to altered serotonergic function (Mann and Stanley 1986). See Table 1 for a summary (Malone and Mann 1993;Owens and Nemeroff 1994;Stoff and Mann 1997;Mann 1998). In major depression there are fewer platelet serotonin transporters (5-HTT), lower CSF 5-HIAA (Mendels et al. 1972;Sjöström and Roos 1972; Ashcroft et al. 1973a Ashcroft et al. , 1973bPost and Goodwin 1974; Bowers 1974; Goodwin and Post 1977;van Praag and de Haan 1979;Koslow et al. 1983; Åsberg et al. 1984; Gerner et al. 1984;Roy et al. 1985;Redmond et al. 1986), as well as a reduced growth hormone (GH) response to 5-hydroxytryptophan (5-HTP) (Upadhyaya et al. 1991) and a blunted prolactin (PRL) response to oral fenfluramine (Siever et al. 1984; Coccaro et al. 1989;O'Keane and Dinan 1991;Mann et al. 1992) and to intravenous L-tryptophan (Heninger et al. 1984; Cowen et al. 1990;Price et al. 1991;Upadhyaya et al. 1991). The antidepressant efficacy of selective serotonin reuptake inhibitors (SSRIs) suggests the abnormality in depression probably includes impaired serotonergic function, because selective enhancement of serotonergic activity is therapeutic (Åsberg et al. 1986a). Depletion of serotonin by parachlorophenylalanine (PCPA) (Shopsin et al. 1976) or by reduction of brain tryptophan (Delgado et al. 1990), quickly reverses the antidepressant effect of serotonergic medication in patients (Åsberg et al. 1986a), suggesting that sustained enhancement of serotonergic function is a necessary requirement to sustain this SSRI-mediated antidepressant effect. It seems that the abnormality in serotonergic function may be a biochemical trait, because a blunted prolactin response to fenfluramine and a vulnerability to depression in response to tryptophan depletion are present during the 24 , NO . 5 period of remission between episodes (Flory et al. 1998). An intermorbid biological abnormality or trait implies a genetic or developmental origin, although enduring illness or treatment effects cannot be ruled out.Lower serotonergic activity is also independently associated with suicidal behavior. We have hypothesized that there is a serotonergic abnormality contributing to the diathesis or vulnerability for suicidal acts (Mann 1998). Lower levels of CSF 5-HIAA (Åsberg et al. 1986b) and a blunted prolactin response to fenfluramine (Mann et al. 1992) correlate with the presence and lethality of past suicide attempts in patients with major depression and can predict future suicide or suicide attempts (Roy et al. 1989;Träskman-Bendz et al. 1992;Nordström et al. 1994). The association between suicide attempts and low CSF 5-HIAA has also been reported in schizophrenia and personality disorders, indicating that this association is independent of diagnosis. Lower brainstem serotonin (5-HT) and/or 5-hydroxyindoleacetic acid (5-HIAA) levels, and alterations in binding kinetics of a number of serotonin receptor subtypes are reported postmortem in the brain of suicide victims compared...

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Relationship Between Central and Peripheral Serotonin Indexes in Depressed and Suicidal Psychiatric Inpatients

Cited by 259 publications

References 19 publications

Low Versus High Prolactin Responders to Fenfluramine Challenge: Marker of Behavioral Differences in Adult Male Cynomolgus Macaques

Low Versus High Prolactin Responders to Fenfluramine Challenge: Marker of Behavioral Differences in Adult Male Cynomolgus Macaques

Association of Serotonin 5-HT2A Receptor Binding and the T102C Polymorphism in Depressed and Healthy Caucasian Subjects

The Neurobiology and Genetics of Suicide and Attempted Suicide: A Focus on the Serotonergic System

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