The interaction between mood and cognitive function studied with PET

Baker, S. C.; Frith, C. D.; Dolan, Raymond J.

doi:10.1017/s0033291797004856

Cited by 211 publications

(115 citation statements)

References 62 publications

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“…These regions share extensive reciprocal connections with the amygdala, anterior temporal and anterior cingulate cortex (Ongur and Price, 2000). Functional neuroimaging studies in healthy subjects have demonstrated a role for the medial and lateral sectors of the IFC in mood regulation (Baker et al, 1997;Northoff et al, 2000) and in emotional memory (Cabeza and Nyberg, 2000). It has been speculated that the IFC is involved in the highest level of behavior regulation, including emotion regulation, through pathways between the IFC and autonomic systems that govern visceral responses associated with affective stimuli (Cabeza and Nyberg, 2000).…”

Section: Discussionmentioning

confidence: 99%

Frontal lobe hypoactivation in medication-free adults with bipolar II depression during response inhibition

Penfold¹,

Vizueta²,

Townsend³

et al. 2015

Psychiatry Research: Neuroimaging

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Section: Discussionmentioning

confidence: 99%

Frontal lobe hypoactivation in medication-free adults with bipolar II depression during response inhibition

Penfold¹,

Vizueta²,

Townsend³

et al. 2015

Psychiatry Research: Neuroimaging

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“…Thalamic activity (serotonin transporters) peaks at 4 h after the injection 24,25 correspondingly. Since previous studies have not revealed significant changes in blood flow either in the hypothalamus/midbrain area or in the thalamus in depressive states 52 ]␤-CIT in prefrontal cortex is low and rather within PET than SPET resolution. 53 The equilibrium state of dopamine transporters in the striatum is reached 16-20 h after the injection.…”

Section: Molecular Psychiatrymentioning

confidence: 94%

Elevated hypothalamic/midbrain serotonin (monoamine) transporter availability in depressive drug-naive children and adolescents

et al. 2000

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Cumulative data suggest depression in adulthood being connected to reduced availability of brain serotonin while the role of dopamine remains less specific. Prospective studies have shown a continuity of depressive episodes from childhood to adulthood, combined with poor social function and excess mortality. The object of this study was to examine whether alterations in brain serotonin and/or dopamine transporter levels are already present in depressive children and adolescents. We examined 41 drug-naive patients (aged 7-17) by single photon emission tomography (SPET) using iodine-123-labelled 2␤-carbomethoxy-3␤(iodophenyl) tropane [ 123 I]␤-CIT as a tracer for monoamine transporters. In addition to the ordinary clinical examination, the patients were given a structured interview and information was gathered from teachers and parents with questionnaires. The diagnoses were established by consensus evaluation between three child psychiatrists. To test the serotonin hypothesis and the dopamine hypothesis regarding depression in children and adolescents, the series was divided into groups with depression present (31) and no depression present (10). In this study, the depressive child and adolescent patients had significantly higher serotonin transporter availability (P Ͻ 0.02) in the hypothalamic/midbrain area. Age did not correlate to the hypothalamic/midbrain serotonin transporter binding ratio. No significant difference in dopamine transporter availability in striatum was found between the depressive and the nondepressive children and adolescents. Molecular Psychiatry (2000) 5, 514-522.

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“…Functional imaging experiments show aberrant perfusion and metabolism in this region of both disorders (Baker et al, 1997;Erkwoh et al, 1997;Haznedar et al, 1997;Rubinsztein et al, 2001), while magnetic resonance studies demonstrate decreased gray matter volume in patients with bipolar disorder (Drevets et al, 1997;Lopez-Larson et al, 2002). At the histopathological level, a reduction in laminar thickness and neuron densities in layers III, V, and VI of ACCx (Bouras et al, 2001) as well as decreases in glial cell density have been reported in ACCx of bipolars (Knable, 1999;Ongur et al, 1998).…”

Section: Introductionmentioning

confidence: 98%

DNA fragmentation is increased in non-GABAergic neurons in bipolar disorder but not in schizophrenia

Buttner

Bhattacharyya

Walsh

et al. 2007

Schizophrenia Research

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Apoptosis is thought to contribute to neuronal loss in bipolar disorder and schizophrenia, although empiric evidence in support of this idea has been lacking. In this study, we investigated whether or not apoptosis is associated with GABAergic interneurons in the anterior cingulate cortex in schizophrenia (n = 14) and bipolar disorder (n = 14) when compared to normal controls (n = 14). A double-labeling technique using the Klenow method of in situ end-labeling (ISEL) of single-stranded DNA breaks was combined with an in situ hybridization localization of mRNA for the 67 kiloDalton (kDa) isoform of glutamate decarboxylase (GAD67) and applied to the anterior cingulate cortex of 14 normal controls, 14 schizophrenics, and 14 patients with bipolar disorder matched for age and postmortem interval. An increase in Klenow-positive, GAD67-negative nuclei was observed in layer V/VI of patients with bipolar disorder, but not schizophrenics. Klenow-positive cells that were also positive for GAD67 mRNA did not show differences in either patient group. Conclusions: This is the first demonstration that there is more DNA fragmentation in cells showing no detectable GAD67 mRNA in patients with bipolar disorder than in schizophrenics or controls. These findings suggest that non-GABAergic cells may be selectively vulnerable to oxidative stress in patients with bipolar disorder.

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The interaction between mood and cognitive function studied with PET

Abstract: Background. Experimentally induced depressed mood is a suggested model for retarded depression. We describe the neural response associated with induced mood and the locus of the interaction between systems mediating mood and cognitive function.

Cited by 211 publications

References 62 publications

Frontal lobe hypoactivation in medication-free adults with bipolar II depression during response inhibition

Frontal lobe hypoactivation in medication-free adults with bipolar II depression during response inhibition

Elevated hypothalamic/midbrain serotonin (monoamine) transporter availability in depressive drug-naive children and adolescents

DNA fragmentation is increased in non-GABAergic neurons in bipolar disorder but not in schizophrenia

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