The Basis for Amine Hypotheses in Affective Disorders

Baldessarini, Ross J.

doi:10.1001/archpsyc.1975.01760270019001

Cited by 159 publications

(32 citation statements)

References 26 publications

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“…In affective disorders, changes have been found in the monoamine concentrations [9], and a reduction in the dopamine metabolite homovanillic acid (HVA) in the CSF has been reported after treatment with antidepres sants [10], It is also known that the GH treatment of nor mal and hypophysectomized rats influences the cerebral concentrations of monoamines [11]. p-Endorphins, which are mainly produced in the pituitary and hypothalamus, have been associated with mood enhancement after exer cise [12].…”

Section: Introductionmentioning

confidence: 99%

Treatment of Growth Hormone-Deficient Adults with Recombinant Human Growth Hormone Increases the Concentration of Growth Hormone in the Cerebrospinal Fluid and Affects Neurotransmitters

Johansson¹,

Larson²,

et al. 1995

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In a double-blind, placebo-controlled trial, the effects of recombinant human growth hormone were studied on cerebrospinal fluid concentrations of growth hormone, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), monoamine metabolites, neuropeptides and endogenous opioid peptides. Twenty patients, 10 patients in each of 2 groups, with adult-onset, growth hormone deficiency were treated for 1 month with recombinant human growth hormone (0.25 U/kg/week) or placebo. All the patients received the appropriate thyroid, adrenal and gonadal hormone replacement. In cerebrospinal fluid, the mean concentration of growth hormone increased from 13.3 ± 4.4 to 149.3 ± 22.2 µU/1 (p = 0.002), during recombinant human growth hormone treatment. The cerebrospinal fluid IGF-1 concentration increased from 0.67 ± 0.04 to 0.99 ± 0.10 µg/1 (p = 0.005) and the IGFBP-3 concentration rose from 13.4 ± 1.25 to 17.5 ± 1.83 µg/l(p = 0.002). The dopamine metabolite homovanillic acid decreased from 282.1 ± 36.0 to 234.3 ± 26.5 nmol/l (p = 0.02) and the vasoactive intestinal peptide decreased from 4.1 ± 0.6 to 3.7 ± 0.4 pmol/l (p = 0.03). Cerebrospinal fluid immunoreactive β-endorphin increased from 24.4 ± 1.8 to 29.9 ± 2.1 pmol/l (p = 0.002). There were no significant changes compared to baseline in the cerebrospinal fluid concentrations of enkephalins, dynorphin A, the norepinephrine metabolite 3-methoxy-4-hydroxyphenyl-ethyleneglycol, the serotonin metabolite 5-hydroxyindoleacetic acid, γ-aminobutyric acid, somatostatin or corticotropin-releasing factor. We conclude that treatment with recombinat human growth hormone causes a tenfold increase in growth hormone in the cerebrospinal fluid, thereby indicating that recombinant human growth hormone passes the blood-cerebrospinal fluid barrier. The cerebrospinal fluid concentrations of IGF-1 and IGFBP-3 increased significantly. Simultaneously, the cerebrospinal fluid concentrations of homovanillic acid and vasoactive intestinal peptide decreased and the concentration of β-endorphin immunoreactivities increased significantly. These changes might explain the improved quality-of-life in patients with growth hormone deficiency following replacement therapy with growth hormone.

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Section: Introductionmentioning

confidence: 99%

Treatment of Growth Hormone-Deficient Adults with Recombinant Human Growth Hormone Increases the Concentration of Growth Hormone in the Cerebrospinal Fluid and Affects Neurotransmitters

Johansson¹,

Larson²,

et al. 1995

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“…Antidepressant activity is assumed to result from the enhancement of central monoaminergic function, which is regarded as deficient in depressed patients (Schildkraut, 1974;Baldessarini, 1975). According to widely accepted hypotheses, the therapeutic efficacy of the known antidepressant drugs is based on a blockage of the inactivation mechanisms of the biogenic amines NA, DA, and/ or 5-HT.…”

Section: Introductionmentioning

confidence: 99%

Studies on brain metabolism of biogenic amines.

Schacht¹,

Leven²,

Bäcker³

1977

Brit J Clinical Pharma

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“…For example, although reserpine and alpha-methlyparatyrosine both reliably induce sedation and psychomotor retar dation in man, only a small proportion of drug treated individuals complain of mental depression (4,5,19,26,52). This highlights a major issue in biological psychiatry -the poor correlation between a given physiological state of con sciousness and its emotional expression.…”

Section: Drug Models Of Mental Illnessmentioning

confidence: 99%

An Amphetamine Model of Manic Depressive Illness

Mamelak¹

1978

Int Pharmacopsychiatry

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Many features of manic-depressive illness can be mimicked in man by the use and withdrawal of amphetamines. In higher doses these drugs induce a syndrome virtually indistinguishable from paranoid schizophrenia. In this paper, some of the biochemical and physiological effects of the amphetamines are examined with the hope of clarifying the nature of the biological changes in these two major functional psychoses. The actions of the amphetamines are shown to reveal the operation of specific homeostatic or adaptive nervous mechanisms. These appear likely also to operate in adaptation to psychological stress. Evidence is presented that these mechanisms are malfunctioning in manic-depressive and acute schizophrenic states and that this accounts for many of the clinical features of these conditions.

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The Basis for Amine Hypotheses in Affective Disorders

Cited by 159 publications

References 26 publications

Treatment of Growth Hormone-Deficient Adults with Recombinant Human Growth Hormone Increases the Concentration of Growth Hormone in the Cerebrospinal Fluid and Affects Neurotransmitters

Treatment of Growth Hormone-Deficient Adults with Recombinant Human Growth Hormone Increases the Concentration of Growth Hormone in the Cerebrospinal Fluid and Affects Neurotransmitters

Studies on brain metabolism of biogenic amines.

An Amphetamine Model of Manic Depressive Illness

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