Dopamine and depression

Abstract

The dopamine hypothesis of schizophrenia and the emphasis on other neurotransmitters, most notably norepinephrine, serotonin, and acetylcholine, in the pathogenesis of depression, have focused attention away from substantial evidence implicating dopamine in affective disorders. The clinical evidence includes alterations in depressive symptoms with aging (concomitant with possible changes in dopamine metabolism), potential dopaminergic involvement in several subtypes of depression, similarities between some of the symptoms of Parkinson's disease and those of depression (including psychomotor retardation and diminished motivation), and potential dopaminergic abnormalities in seasonal mood disorder. The biochemical evidence in patients with depression derives from studies of homovanillic acid, a dopamine metabolite, indicating diminished dopamine turnover. In addition, there is a considerable amount of pharmacologic evidence regarding the efficacy of antidepressants with dopaminergic effects in the treatment of depression. We conclude that dopamine likely contributes significantly to the pathophysiology of depression. However, the role of dopamine in this syndrome must be understood in the context of existing theories involving other neurotransmitters which may act independently, and interact with dopamine and other neurochemicals, to contribute to depression.

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

“…In agreement, a number of studies have shown that there is a reduced level of DA and its metabolites in the CSF of depressed patients (Brown and Gershon, 1993) and also a reduced release and metabolism of DA in the basal ganglia of animals subjected to stressors that induce behavioral depression (Cabib and Puglisi-Allegra, 1996). This reduction, however, does not appear to be caused by a direct impairment of the dopaminergic neurons or postsynaptic receptors themselves (Weiss et al, 1996;Cabib et al, 1998;Ossowska et al, 2001;Herman et al, 1984;ZebrowskaLupina et al, 1988), but may occur instead in an afferent system that modulates dopaminergic function.…”

Amphetamine Primes Motivation to Gamble and Gambling-Related Semantic Networks in Problem Gamblers

“…There is a high comorbidity with each of these factors and problem gambling Specker et al, 1995). Moreover, each of these disorders involves disturbances in neurochemical systems activated by psychostimulant drugs (Brown and Gershon, 1993;Solanto, 2002). Therefore, it remains to be determined if the present findings extend to such cases.…”

Therapeutic Benefits of Laughter in Mental Health: A Theoretical Review

“…A positive mood can be gained through the forced laugh, and a bad mood, personality, or thought can be changed somewhat into a positive direction (Isen and Means 1983). According to the latest precedent studies, reduction in secretion of the neurotransmitters, dopamine and serotonin, is the representative of one of the many causes of depression; therefore, if the secretion of those substances reduces, there will be a disorder in mood control in the brain and depression will develop (Brown and Gershon 1993). However, a positive attitude and forced laughter can help maintain dopamine activity (Ashby et al 1999).…”