“…Interestingly, it has been proposed that an increase in dopamine activity induced by chronic antidepressant treatments is one of the mechanisms of action underlying the efficacy of these compounds, since their effects are antagonized by low doses of D 2 /D 3 antagonists (Borsini et al, 1984;Borsini et al, 1985a, b;Pulvirenti and Samanin, 1986;Sampson et al, 1991;Serra et al, 1992;D'Aquila et al, 2000a). Moreover, antidepressant treatments are associated with increased dopaminergic function in the mesolimbic system and increased behavioral response to dopamine agonists (Spyraki and Fibiger, 1981;Maj et al, 1984a, b;Cervo and Samanin, 1987;De Montis et al, 1990;Ainsworth et al, 1998a;D'Aquila et al, 2000bD'Aquila et al, , 2003, which takes place after chronic treatment (2-3 weeks), a period of time that correlates with that necessary for the onset of antidepressant activity in the clinic.…”
“…Interestingly, it has been proposed that an increase in dopamine activity induced by chronic antidepressant treatments is one of the mechanisms of action underlying the efficacy of these compounds, since their effects are antagonized by low doses of D 2 /D 3 antagonists (Borsini et al, 1984;Borsini et al, 1985a, b;Pulvirenti and Samanin, 1986;Sampson et al, 1991;Serra et al, 1992;D'Aquila et al, 2000a). Moreover, antidepressant treatments are associated with increased dopaminergic function in the mesolimbic system and increased behavioral response to dopamine agonists (Spyraki and Fibiger, 1981;Maj et al, 1984a, b;Cervo and Samanin, 1987;De Montis et al, 1990;Ainsworth et al, 1998a;D'Aquila et al, 2000bD'Aquila et al, , 2003, which takes place after chronic treatment (2-3 weeks), a period of time that correlates with that necessary for the onset of antidepressant activity in the clinic.…”
“…In addition, another study provided support for the supposition that noradrenergic transmission is necessary for motivated behaviors (Jasmin al, 2006). Imipramine has been shown in animal studies to affect both the dopaminergic (De Montis et al, 1990) and noradrenergic system (Linner et al, 1999).…”
Section: Emotional Processes and Biological Systemsmentioning
Depression has often been associated with increased negative affect reactivity to stress (Stress-Sensitivity) and reduced capacity to experience pleasure or positive affect (Reward Experience). To date, no studies have prospectively examined changes in StressSensitivity and Reward Experience following antidepressant treatment. The sample included 83 depressed patients and 22 healthy controls. A randomized controlled trial was carried out with patients receiving either imipramine or placebo for 6 weeks. At baseline and 6 weeks, patients and controls participated in an Experience Sampling procedure, prospectively measuring ecologically valid daily life appraisals of activities and mood states. The course of depression was assessed with the Hamilton Depression Rating Scale (HDRS). Multilevel linear regression analyses showed that patients had higher negative and lower positive appraisals of activities than controls. In addition, patients showed increased Stress-Sensitivity (negative affect reactivity to negatively appraised activities). Treatment with imipramine decreased Stress-Sensitivity and increased Reward Experience (positive affect reactivity to positively appraised activities). Changes in Stress-Sensitivity and Reward Experience were in part reducible to changes in the process of activity appraisal itself. However, increase in Reward Experience, but not decrease in Stress-Sensitivity, discriminated between patients who responded and those who did not, independent of changes in the process of activity appraisal itself. Response to treatment in depression may be conditional on restoration of hedonic capacity, the cerebral substrate of which requires further study in relation to antidepressant response. A search for (synergistic) antidepressant therapies specifically targeting ability to experience reward may be warranted.
“…12 Imipramine and its active metabolite desimipramine block [ 3 H]-dopamine uptake in the limbic regions and not in striatum, and imipramine also induces reduction of DOPAC levels, a dopamine metabolite, in the same cerebral region. 56 It seems that chronic treatment with some antidepressants causes down-regulation of D1-receptors in the limbic area whereas a decreased number of receptors is less evident in the striatum. 56 In addition to enhanced responsiveness of D2/D3 receptors, antidepressants act by desensitizing dopamine D2 presynaptic autoreceptors although it is possible that this effect may be developed as a withdrawal effect following long-term treatment.…”
Section: The Action Of Antidepressant Drugs On Monoaminergic Transmismentioning
confidence: 99%
“…56 It seems that chronic treatment with some antidepressants causes down-regulation of D1-receptors in the limbic area whereas a decreased number of receptors is less evident in the striatum. 56 In addition to enhanced responsiveness of D2/D3 receptors, antidepressants act by desensitizing dopamine D2 presynaptic autoreceptors although it is possible that this effect may be developed as a withdrawal effect following long-term treatment. 12 The development of hypersensitivity in striatal postsynaptic dopamine receptors has been the most prominent theory explaining the pathophysiology of TD.…”
Section: The Action Of Antidepressant Drugs On Monoaminergic Transmismentioning
Depression is the most prevalent functional psychiatric disorder in late life. The problem of motor disorders associated with antidepressant use is relevant in the elderly. Elderly people are physically more frail and more likely to be suffering from physical illness, and any drug given may exacerbate pre-existing diseases, or interact with other drug treatments being administered for physical conditions. Antidepressants have been reported to induce extrapyramidal symptoms, including parkinsonism. These observations prompted us to review the neurobiological mechanism that may be involved in this complex interplay including neurotransmitters and neuronal circuits involved in movement and emotion control and their changes related to aging and disease. The study of the correlations between motor and mood disorders and their putative biochemical bases, as presented in this review, provide a rationale either to understand or to foresee motor side effects for psychotropic drugs, in particular antidepressants. Molecular Psychiatry (2001) 6, 134-142.
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