Role of the dopaminergic system in depression

Kapur, Shitij; Mann, J. John

doi:10.1016/0006-3223(92)90137-o

Cited by 323 publications

(171 citation statements)

References 94 publications

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“…Several studies fmd decreased cerebrospinal fluid homovanillic acid in patients with depression (Goodwin et al 1973;Randrup et al 1975;van Praag et al 1975). However, because this abnormality is most pr onounced in patients with psychomotor retardation (Kapur and Mann 1992), it is unclear whether low cerebrospinal fluid homovanillic acid is related to depression itself or to accompanying psychomotor retardation. The questions regarding the relationship be tween DA and depression are compounded by the fact that most studies using DA agonists as neuroen do crine challenge agents do not fmd evidence of ab normal DA function in depression (Costain et al 1982;Christie et al 1982, Balldin et al 1982).…”

Section: Resultsmentioning

confidence: 99%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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We administered the serotonin-1a agonist buspirone (0.4 mglkg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III -R major depressive disorder (MOD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between KEY WORDS: Depressive disorder; Serotonin; Buspirone; Prolactin 655 Avenue of the Americas, New York, NY 10010 placebo corrected-peak prolactin level and severity of depression or suicidality. There was a nonsignificant trend for the melancholic (n = 5) depressed patients to have a lower placebo corrected-peak prolactin level than nonmelancholic depressed patients (n = B).Our findings support a role for the serotonin-1a receptor in the etiology of MOD, specifically at the postsynaptic site. and 5-HT -releasing agents (Siever et al. 1984; Coccaro et al. 1989;Mitchell and Smythe 1990;Lichtenberg et al. 1992;Shapira et al. 1992aShapira et al. , 1992b.There has been a relatively consistent ii.nding of de creased prolactin response to various serotonergic agents in subjects with major depressive disorder (MOD) using nonspecific 5-HT challenge agents; thus, recent research has focused on the role of specific subtypes

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Section: Resultsmentioning

confidence: 99%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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“…Dopaminergic deficits are associated with several psychiatric symptoms in man, such as depression (Kapur and Mann, 1992;Fibiger, 1995;Pania and Gessab, 2002). A deficiency of mesolimbic dopaminergic pathway plays a critical role for the etiology of symptoms of depression like anhedonia and decreased motivation (Willner, 1983b;Schultz, 1997;Berridge and Robinson, 1998;Naranjo et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Antidepressant-Like Effect of D2/3 Receptor-, but not D4 Receptor-Activation in the Rat Forced Swim Test

Basso

Gallagher

Bratcher

et al. 2005

Neuropsychopharmacol

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“…45 In fact, results from studies in depression, Parkinson's disease and animal models of depression suggest deficiency of dopamine as the model of depression has a very high probability. 46 Depressive symptoms have previously correlated inversely to dopamine transporter availability in alcoholics. 47 There are no previous studies on brain dopamine activity in depressive children, but dopamine-active drugs have a well proven, serotonin-mediated effect on the symptoms of attention deficit hyperactivity disorder.…”

Section: Molecular Psychiatrymentioning

confidence: 99%

Elevated hypothalamic/midbrain serotonin (monoamine) transporter availability in depressive drug-naive children and adolescents

et al. 2000

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Cumulative data suggest depression in adulthood being connected to reduced availability of brain serotonin while the role of dopamine remains less specific. Prospective studies have shown a continuity of depressive episodes from childhood to adulthood, combined with poor social function and excess mortality. The object of this study was to examine whether alterations in brain serotonin and/or dopamine transporter levels are already present in depressive children and adolescents. We examined 41 drug-naive patients (aged 7-17) by single photon emission tomography (SPET) using iodine-123-labelled 2␤-carbomethoxy-3␤(iodophenyl) tropane [ 123 I]␤-CIT as a tracer for monoamine transporters. In addition to the ordinary clinical examination, the patients were given a structured interview and information was gathered from teachers and parents with questionnaires. The diagnoses were established by consensus evaluation between three child psychiatrists. To test the serotonin hypothesis and the dopamine hypothesis regarding depression in children and adolescents, the series was divided into groups with depression present (31) and no depression present (10). In this study, the depressive child and adolescent patients had significantly higher serotonin transporter availability (P Ͻ 0.02) in the hypothalamic/midbrain area. Age did not correlate to the hypothalamic/midbrain serotonin transporter binding ratio. No significant difference in dopamine transporter availability in striatum was found between the depressive and the nondepressive children and adolescents. Molecular Psychiatry (2000) 5, 514-522.

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Role of the dopaminergic system in depression

Cited by 323 publications

References 94 publications

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Antidepressant-Like Effect of D2/3 Receptor-, but not D4 Receptor-Activation in the Rat Forced Swim Test

Elevated hypothalamic/midbrain serotonin (monoamine) transporter availability in depressive drug-naive children and adolescents

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