Single photon emission computerized tomography assessment of cerebral dopamine D2 receptor blockade in depression before and after sleep deprivation—preliminary results

Ebert, Dieter; Feistel, H.; Kaschka, Wolfgang P.; Barocka, Arnd; Pirner, A

doi:10.1016/0006-3223(94)90024-8

Cited by 129 publications

(47 citation statements)

References 34 publications

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“…In contrast, pretreatment with the dopamine agonist, amineptine, prevents the antidepressant effects of TSD (Benedetti et al, 1996). TSD also seems to activate limbic dopaminergic pathways which can be measured in increased limbic blood flow, increased D2 dopamine receptor occupancy, and increased eye-blink rates after TSD treatment (Ebert et al, 1994a;Ebert et al, 1994b;Ebert et al, 1996). These results, and the significant similarities between the feelings induced by TSD and psychostimulant use, have implicated the limbic dopaminergic system in the therapeutic actions of TSD (Ebert and Berger, 1998).…”

Section: Treating Mood Disorders By Altering the Circadian Cycle 41 mentioning

confidence: 99%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

585

386

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For many years, researchers have suggested that abnormalities in circadian rhythms may underlie the development of mood disorders such as bipolar disorder, major depression and seasonal affective disorder. Furthermore, some of the treatments that are currently employed to treat mood disorders are thought to act by shifting or "resetting" the circadian clock, including total sleep deprivation and bright light therapy. There is also reason to suspect that many of the mood stabilizers and antidepressants used to treat these disorders may derive at least some of their therapeutic efficacy by affecting the circadian clock. Recent genetic, molecular and behavioral studies implicate individual genes that make up the clock in mood regulation. As well, important functions of these genes in brain regions and neurotransmitter systems associated with mood regulation is becoming apparent. In this review, the evidence linking circadian rhythms and mood disorders, and what is known about the underlying biology of this association, is presented.

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Section: Treating Mood Disorders By Altering the Circadian Cycle 41 mentioning

confidence: 99%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

585

386

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“…Molecular imaging studies of nonpharmacological interventions have only been performed for total sleep deprivation. 56 The therapeutic success of sleep deprivation was associated with lower binding of a dopamine D2 receptor ligand and thus higher dopamine release, and with reduction in cingulate perfusion. Reduced ACC glucose metabolism was also observed in patients with MDD who responded to IPT.…”

Section: Molecular Mechanisms Of Psychotherapymentioning

confidence: 99%

How psychotherapy changes the brain – the contribution of functional neuroimaging

2006

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A thorough investigation of the neural effects of psychotherapy is needed in order to provide a neurobiological foundation for widely used treatment protocols. This paper reviews functional neuroimaging studies on psychotherapy effects and their methodological background, including the development of symptom provocation techniques. Studies of cognitive behavioural therapy (CBT) effects in obsessive-compulsive disorder (OCD) were consistent in showing decreased metabolism in the right caudate nucleus. Cognitive behavioural therapy in phobia resulted in decreased activity in limbic and paralimbic areas. Interestingly, similar effects were observed after successful intervention with selective serotonin reuptake inhibitors (SSRI) in both diseases, indicating commonalities in the biological mechanisms of psycho-and pharmacotherapy. These findings are discussed in the context of current neurobiological models of anxiety disorders. Findings in depression, where both decreases and increases in prefrontal metabolism after treatment and considerable differences between pharmacological and psychological interventions were reported, seem still too heterogeneous to allow for an integrative account, but point to important differences between the mechanisms through which these interventions attain their clinical effects. Further studies with larger patient numbers, use of standardised imaging protocols across studies, and ideally integration with molecular imaging are needed to clarify the remaining contradictions. This effort is worthwhile because functional imaging can then be potentially used to monitor treatment effects and aid in the choice of the optimal therapy. Finally, recent advances in the functional imaging of hypnosis and the application of neurofeedback are evaluated for their potential use in the development of psychotherapy protocols that use the direct modulation of brain activity as a way of improving symptoms.

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“…Animal and human studies show that the dopaminergic system has an important role in modulating the prefrontal activation during working memory. [63][64][65][66] The dysfunction of the frontal cortex systems in subjects with MDD was reported in positron emission tomography and single photon emission tomography studies, [67][68][69][70] although there is no study, to our knowledge, that investigated the direct relation between the dopaminergic system and working memory in MDD patients. The dysfunction of the dopaminergic system in MDD patients may underlie the abnormal function of the frontolimbic network in the process of working memory reported in our present study and others.…”

Section: Working Memory In Depression K Matsuo Et Almentioning

confidence: 99%

“…The dysfunction of the dopaminergic system in MDD patients may underlie the abnormal function of the frontolimbic network in the process of working memory reported in our present study and others. [67][68][69][70] Our study has some methodological limitations, including the relatively modest sample size and the fact that our sample included patients with comorbid anxiety disorders. The ACC activation we observed in the MDD patients may include the influence of anxiety symptoms, because the anatomical pathophysiology of anxiety disorders involves the hippocampus, amygdala and ACC, [71][72][73] and patients with anxiety disorders also show a deficit of working memory.…”

Section: Working Memory In Depression K Matsuo Et Almentioning

confidence: 99%

Prefrontal hyperactivation during working memory task in untreated individuals with major depressive disorder

et al. 2006

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The prefrontal cortex, a part of the limbic-thalamic-cortical network, participates in regulation of mood, cognition and behavior and has been implicated in the pathophysiology of major depressive disorder (MDD). Many neuropsychological studies demonstrate impairment of working memory in patients with MDD. However, there are few functional neuroimaging studies of MDD patients during working memory processing, and most of the available ones included medicated patients or patients with both MDD and bipolar disorder. We used functional magnetic resonance imaging (fMRI) to measure prefrontal cortex function during working memory processing in untreated depressed patients with MDD. Fifteen untreated individuals with Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition recurrent MDD (mean age7s.d. = 34.3711.5 years) and 15 healthy comparison subjects (37.7712.1 years) matched for age, sex and race were studied using a GE/Elscint 2T MR system. An echo-planar MRI sequence was used to acquire 24 axial slices. The n-back task (0-back, 1-back and 2-back) was used to elicit frontal cortex activation. Data were analyzed with a multiple regression analysis using the FSL-FEAT software. MDD patients showed significantly greater left dorsolateral cortex activation during the n-back task compared to the healthy controls (P < 0.01), although task performance was similar in the two groups. Furthermore, the patients showed significant anterior cingulate cortex activation during the task, but the comparison subjects did not (P < 0.01). This study provides in vivo imaging evidence of abnormal frontolimbic circuit function during working memory processing in individuals with MDD.

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Single photon emission computerized tomography assessment of cerebral dopamine D2 receptor blockade in depression before and after sleep deprivation—preliminary results

Cited by 129 publications

References 34 publications

Circadian genes, rhythms and the biology of mood disorders

Circadian genes, rhythms and the biology of mood disorders

How psychotherapy changes the brain – the contribution of functional neuroimaging

Prefrontal hyperactivation during working memory task in untreated individuals with major depressive disorder

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