Positron Emission Tomography Measurement of Cerebral Metabolic Correlates of Tryptophan Depletion—Induced Depressive Relapse

Bremner, J. Douglas; Innis, Robert B.; Salomon, Ronald M.; Staib, Lawrence H.; Ng, Chin K.; Miller, Helen; Bronen, Richard A.; Krystal, John H.; Duncan, Jeremy W.; Rich, D. R.; Price, Lawrence H.; Malison, Robert T.; Dey, Holley M.; Soufer, Robert; Charney, Dennis S.

doi:10.1001/archpsyc.1997.01830160092012

Cited by 249 publications

(164 citation statements)

References 75 publications

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“…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. A comparable pattern of abnormality in the orbitofrontal cortical region is seen in refractory depressed patients (Mayberg et al, 1997) and in patients with depression associated with neurological disorders (Bromfield et al, 1992;Mayberg et al, 1990Mayberg et al, , 1992.…”

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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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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“…Only change scores of the HRSD and plasma Trp levels were available in the study by Bremner et al (1997). These patients could therefore not be included in linear regression analyses.…”

Section: Missing Datamentioning

confidence: 99%

“…In Spillman et al (2001), , and Bremner et al(1997), a clinically significant recurrence in depressive symptoms after ATD (i.e. responder to ATD: depressive 'relapse') was explicitly defined.…”

Section: Computation Of Statistically Comparable Mood Scoresmentioning

confidence: 99%

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Predictors of Mood Response to Acute Tryptophan Depletion A Reanalysis

Booij

Does

Benkelfat

et al. 2002

Neuropsychopharmacology

166

134

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Acute tryptophan depletion (ATD) induces depressive symptoms in 50-Acute tryptophan depletion (ATD) is a technique used to study serotonin (5-hydroxytryptamine; 5-HT) brain function in mood disorders. In this paradigm, 5-HT function is temporarily lowered by deprivation of its precursor L -Tryptophan (Trp), an amino acid essential for 5-HT synthesis. It has been suggested that behavioral response to ATD might be informative about the pathophysiology of clinical depression and the mechanisms mediating antidepressant efficacy.A number of studies have demonstrated that ATD temporarily induces depressive symptoms in remitted depressive patients treated with antidepressant medication (Delgado et al. 1990; Spillman et al. 2001). The recurrence of symptoms appears to be highest in subjects treated with a selective serotonin reuptake inhibitor (SSRI) (Delgado et al. 1990(Delgado et al. , 1994(Delgado et al. , 1999.However, not all patients react to ATD; even in SSRItreated patients, ATD exacerbates symptoms in 50-60% of investigated patients (Van der Does 2001a). This raises the question of what factors determine response to ATD. It has been argued that induced depressive

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“…Indeed, clinical evidence indicates that reduction of brain 5-HT levels, induced by a dietary depletion of L-tryptophan, can reverse the antidepressant action of selective 5-HT reuptake inhibitors (SSRI), monoamine oxidase inhibitors (MAOIs), and the a 2 -adrenoceptor antagonist mirtazapine (Bremner et al, 1997;Nishizawa et al, 1997;Moreno et al, 2000). Preclinical studies show that antidepressant treatments increase 5-HT neurotransmission with a time course that is consistent with their delayed therapeutic effect.…”

Section: Introductionmentioning

confidence: 99%

Effects of Acute and Long-Term Administration of Escitalopram and Citalopram on Serotonin Neurotransmission: an In Vivo Electrophysiological Study in Rat Brain

Mansari

Sanchéz

Chouvet

et al. 2005

Neuropsychopharmacol

179

102

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The present study was undertaken to compare the acute and long-term effects of escitalopram and citalopram on rat brain 5-HT neurotransmission, using electrophysiological techniques. In hippocampus, after 2 weeks of treatment with escitalopram (10 mg/kg/day, s.c.) or citalopram (20 mg/kg/day, s.c.), the administration of the selective 5-HT 1A receptor antagonist WAY-100,635 (20-100 mg/kg, i.v.) dose-dependently induced a similar increase in the firing activity of dorsal hippocampus CA 3 pyramidal neurons, thus revealing direct functional evidence of an enhanced tonic activation of postsynaptic 5-HT 1A receptors. In dorsal raphe nucleus, escitalopram was four times more potent than citalopram in suppressing the firing activity of presumed 5-HT neurons (ED 50 ¼ 58 and 254 mg/kg, i.v., respectively). Interestingly, the suppressant effect of escitalopram (100 mg/kg, i.v.) was significantly prevented, but not reversed by R-citalopram (250 mg/kg, i.v.). Sustained administration of escitalopram and citalopram significantly decreased the spontaneous firing activity of presumed 5-HT neurons. This firing activity returned to control rate after 2 weeks in rats treated with escitalopram, but only after 3 weeks using citalopram, and was associated with a desensitization of somatodendritic 5-HT 1A autoreceptors. These results suggest that the time course of the gradual return of presumed 5-HT neuronal firing activity, which was reported to account for the delayed effect of SSRI on 5-HT transmission, is congruent with the earlier onset of action of escitalopram vs citalopram in validated animal models of depression and anxiety.

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Positron Emission Tomography Measurement of Cerebral Metabolic Correlates of Tryptophan Depletion—Induced Depressive Relapse

Abstract: Specific brain regions, including the middle frontal gyrus, thalamus, and orbitofrontal cortex, may mediate the symptoms of patients with major depression.

Cited by 249 publications

References 75 publications

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

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

Predictors of Mood Response to Acute Tryptophan Depletion A Reanalysis

Effects of Acute and Long-Term Administration of Escitalopram and Citalopram on Serotonin Neurotransmission: an In Vivo Electrophysiological Study in Rat Brain

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