Effect of sertraline on regional metabolic rate in patients with affective disorder

Buchsbaum, Monte S.; Wu, Joseph C.; Siegel, Benjamin V.; Hackett, Elizabeth; Trenary, Mignon; Abel, Lennart; Reynolds, Chandra A.

doi:10.1016/s0006-3223(96)00097-2

Cited by 284 publications

(168 citation statements)

References 40 publications

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“…The finding that low-current electrical stimulation of the rat medial PFC enhances 5-HT output in such limbic structures as the hippocampus and amygdala underlines the importance of the medial PFC for pathophysiology and treatment of depression. Prefrontal abnormalities in depressed patients were found mostly in the medial parts of PFC (Drevets et al 1997;Ebert and Ebmeier 1996;Mann et al 1996;Buchsbaum et al 1997;Agren and Reibring 1994). It was suggested that one of the core symptoms of depression, namely, motor and affective apathy, is related specifically to dysfunctions of the medial PFC (Cummings 1995;Saint-Cyr et al 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Both neuropsychological and oculomotor functioning of prefrontal cortex is impaired in depression (Goodwin 1997;Sweeney et al 1998). Furthermore, symptom improvement and remission of depressed patients have been associated with increases in cerebral blood flow and glucose metabolism in this region (Goodwin et al 1993;Bench et al 1995;Bonne and Krausz 1997;Buchsbaum et al 1997 NO . 3 This close association between prefrontal cortical dysfunction and depression suggests that enhancement of PFC activity might be beneficial in the treatment of this disorder.…”

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confidence: 99%

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Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Juckel

1999

Neuropsychopharmacology

103

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Decreased activity of the prefrontal cortex (PFC), as well as reduced serotonergic neurotransmission, is considered as a characteristic feature of major depression. The mechanism by which electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS) achieve their antidepressant effects may involve changes in PFC activity. It is, however, still unclear whether these changes are accompanied by increased synaptic availability of serotonin (5-HT). In the present study, 5-HT efflux in the rat ventral hippocampus and amygdala was analyzed using in vivo microdialysis during low-current electrical stimulation of PFC and other cortical regions. Electrical stimulation of the medial PFC produced current-dependent increases in limbic 5-HT output in both urethane-anesthetized and behaving rats. No effects on 5-HT levels were seen after comparable stimulation of either the lateral parts of the PFCAn extensive body of clinical evidence suggests that prefrontal cortex (PFC) abnormalities are involved in the pathophysiology of major depression. Significantly decreased cerebral blood flow as well as reduced rates of glucose metabolism have been consistently found in the PFC of depressed patients (Soares and Mann 1997;Kennedy et al. 1997;George et al. 1993). This reduction seems to be localized predominantly in the left hemisphere (Baxter et al. 1989;Martinot et al. 1990). This is supported by structural neuroimaging studies demonstrating that poststroke depression is more likely to occur following a lesion in the left PFC rather than either in the right PFC or elsewhere in the left hemisphere (Morris et al. 1996;Robinson et al. 1984). Both neuropsychological and oculomotor functioning of prefrontal cortex is impaired in depression (Goodwin 1997;Sweeney et al. 1998). Furthermore, symptom improvement and remission of depressed patients have been associated with increases in cerebral blood flow and glucose metabolism in this region (Goodwin et al. 1993;Bench et al. 1995;Bonne and Krausz 1997;Buchsbaum et al. 1997 NO . 3 This close association between prefrontal cortical dysfunction and depression suggests that enhancement of PFC activity might be beneficial in the treatment of this disorder. Consistent with this idea, electroconvulsive therapy (ECT), as well as transcranial magnetic stimulation (TMS), seems to achieve its antidepressant effects by altering PFC activity. ECT leads to pronounced prefrontal EEG changes, which are directly related to the therapeutic outcome. Hence, the efficacy of ECT seems to be critically linked to prefrontal cortex involvement in ECT-induced seizure activity (Sackeim et al. 1996). This is further supported by studies that have reported changes in cerebral blood flow in prefrontal cortex of ECT responders (Nobler et al. 1994;Bonne et al. 1996;Petracca et al. 1995). In recent years, repetitive TMS of the left dorsolateral prefrontal cortex has emerged as a successful antidepressant treatment (Pascual-Leone et al. 1996;George et al. 1997). Although the exact mechanism underlying the ef...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Juckel

1999

Neuropsychopharmacology

103

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“…Furthermore, recent data suggest (Heckers et al, 2002) that bipolar disorder is associated with a significant decrease of glutamic acid decarboxylase (GAD) mRNA-positive neurons and of GAD 65 mRNA expression in the hippocampus. Pharmacotherapeutic studies have also reported increased regional activation of the left prefrontal cortex, thalamus, and medial frontal gyrus post-treatment in depressed patients (Baxter et al, 1989;Bench et al, 1995;Buchsbaum et al, 1997;Mayberg et al, 1999;Saxena et al, 2002). Taken together, these findings indicate that there are abnormalities of the limbic system in depressed patients.…”

Section: What Might This Study Tell Us About Ltg's Mechanism Of Actiomentioning

confidence: 91%

Interleaved Transcranial Magnetic Stimulation/Functional MRI Confirms that Lamotrigine Inhibits Cortical Excitability in Healthy Young Men

Tenebäck

Nahas

et al. 2004

Neuropsychopharmacol

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Little is known about how lamotrigine (LTG) works within brain circuits to achieve its clinical effects. We wished to determine whether the new technique of interleaved transcranial magnetic stimulation (TMS)/functional magnetic resonance imaging (fMRI) could be used to assess the effects of LTG on activated motor or prefrontal/limbic circuits. We carried out a randomized, double-blind, crossover trial involving two visits 1 week apart with TMS measures of cortical excitability and blood oxygen level-dependent TMS/fMRI. Subjects received either a single oral dose of 325 mg of LTG or placebo on each visit. In all, 10 subjects provided a complete data set that included interleaved TMS/fMRI measures and resting motor threshold (rMT) determinations under both placebo and LTG conditions. A further two subjects provided only rMT data under the two drug conditions. LTG caused a 14.979.6% (mean7SD) increase in rMT 3 h after the drug, compared with a 0.6710.9% increase 3 h after placebo (t ¼ 3.41, df ¼ 11, po0.01). fMRI scans showed that LTG diffusely inhibited cortical activation induced by TMS applied over the motor cortex. In contrast, when TMS was applied over the prefrontal cortex, LTG increased the TMS-induced activation of limbic regions, notably the orbitofrontal cortex and hippocampus. These results suggest that LTG, at clinically relevant serum concentrations, has a general inhibitory effect on cortical neuronal excitability, but may have a more complex effect on limbic circuits. Furthermore, the interleaved TMS/fMRI technique may be a useful tool for investigating regional brain effects of psychoactive compounds.

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“…Alternatively, the effects of depression in this area may overpower those of impulsivity in BPD as some functional imaging studies have also suggested a role for the orbital prefrontal cortex in the pathophysiology of depression. For example, studies that examined abnormalities during a Major Depressive Episode and after various forms of treatment report normalization of orbitofrontal and anterior cingulate abnormalities with treatment (Baxter Jr et al, 1989;Bench et al, 1995;Brody et al, 1999;Buchsbaum et al, 1997;Mayberg et al, 2000Mayberg et al, , 2002. Indeed, Bremner et al (1997) found that depressed patients who were 6 weeks into a course of antidepressant treatment exhibited decreases in glucose metabolic rates in the orbitofrontal cortex and thalamus after a tryptophan-depletion-induced acute relapse compared to patients without depressive symptoms.…”

Section: Orbitofrontal Cortex In Mdd With Bpd Compared To Mddmentioning

confidence: 99%

Positron Emission Tomography of Regional Brain Metabolic Responses to a Serotonergic Challenge in Major Depressive Disorder with and without Borderline Personality Disorder

Oquendo

Krunic

Parsey

et al. 2005

Neuropsychopharmacol

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Previous neuroimaging studies of major depression have not controlled for the presence of personality disorders characterized by impulsive aggressive behavior, such as borderline personality disorder (BPD). Using positron emission tomography (PET), we studied regional glucose uptake in response to fenfluramine (FEN) in depressed subjects with BPD (n ¼ 11) and depressed patients without Cluster B Axis II disorders (n ¼ 8). Subjects were scanned while medication-free after a single blind placebo administration and after FEN on a second day. Brain responses were measured by PET imaging of [ 18 F]fluorodeoxyglucose (FDG) and serial prolactin levels. Scans were compared at a voxel level using statistical parametric mapping. Correlations of changes in relative regional cerebral uptake (rCMRglu) with clinical measures were assessed. Depressed borderline patients had greater relative activity in parietotemporal cortical regions (BA 40, BA 22, and BA 42) before and after FEN activation compared to those without BPD. They also had less relative uptake in the anterior cingulate cortex (BA 32) at baseline compared to depressed patients without BPD and FEN abolished this difference. Impulsivity was positively correlated with rCMRglu in superior and middle frontal cortex (BA 6 and 44). Hostility was positively correlated with rCMRglu in temporal cortical regions (BA 21 and 22). In conclusions, borderline pathology in the context of a Major Depressive Disorder is associated with altered activity in parietotemporal and anterior cingulate cortical regions. Controlling for the presence of BPD in future imaging studies of mood disorders may elucidate similarities and differences in regional serotonergic function in these two often comorbid disorders.

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Effect of sertraline on regional metabolic rate in patients with affective disorder

Cited by 284 publications

References 40 publications

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Interleaved Transcranial Magnetic Stimulation/Functional MRI Confirms that Lamotrigine Inhibits Cortical Excitability in Healthy Young Men

Positron Emission Tomography of Regional Brain Metabolic Responses to a Serotonergic Challenge in Major Depressive Disorder with and without Borderline Personality Disorder

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