Glial reduction in amygdala in major depressive disorder is due to oligodendrocytes

Hamidi, Massihullah; Drevets, Wayne C.; Price, Joseph L.

doi:10.1016/j.biopsych.2003.11.006

Cited by 324 publications

(255 citation statements)

References 56 publications

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“…A reduction in the size of neuronal cell bodies has also been observed in the hippocampus of patients with depression . Decreased glial density has also been reported in the amygdala (Bowley et al, 2002;Hamidi et al, 2004) supporting the involvement of the amygdala in depression. These studies indicate that major depression is related to impairments in structural plasticity and cellular atrophy (Duman, 2004).…”

Section: Introductionmentioning

confidence: 69%

“…Because of the anatomical and functional connections between the DG and the amygdala, abnormal modulation of hippocampal-amygdala pathways may contribute to chronically hypersensitive stress and fear responses (McEwen, 2005). Postmortem studies have shown significant reductions in oligodendrocyte density and glia/ neuron ratio in the amygdala of individuals with major depressive disorder, without a change in neuronal density (Hamidi et al, 2004). In our study, there was no effect of stress on Bax, suggesting that the effects of stress are not mediated by regulation of mRNA of this proapoptotic factor.…”

Section: Discussionmentioning

confidence: 99%

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Repeated Unpredictable Stress and Antidepressants Differentially Regulate Expression of the Bcl-2 Family of Apoptotic Genes in Rat Cortical, Hippocampal, and Limbic Brain Structures

Kosten

Galloway

Duman

et al. 2007

Neuropsychopharmacol

147

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Apoptosis has been proposed as a contributing cellular mechanism to the structural alterations that have been observed in stress-related mood disorders. Antidepressants, on the other hand, are hypothesized to exert trophic and/or neuroprotective actions. The present study examined the regulation of the major antiapoptotic (Bcl-2, Bcl-xl) and proapoptotic (Bax) genes by repeated unpredictable stress (an animal model of depression) and antidepressant treatments (ADT). In adult rats, exposure to unpredictable stress reduced Bcl-2 mRNA levels in the central nucleus of the amygdala (CeA), cingulate (Cg), and frontal (Fr) cortices. Bcl-xl mRNA was significantly decreased in hippocampal subfields. In contrast, chronic administration of clinically effective antidepressants from four different classes, ie fluoxetine, reboxetine, tranylcypromine, and electroconvulsive seizures (ECS) upregulated Bcl-2 mRNA expression in the Cg, Fr, and CeA. Reboxetine, tranylcypromine, and ECS selectively increased Bcl-xl, but not Bcl-2 mRNA expression in the hippocampus. Chemical ADT but not ECS, robustly enhanced Bcl-2 expression in the medial amygdaloid nucleus and ventromedial hypothalamus. Fluoxetine did not influence Bcl-xl expression in the hippocampus, but it was the only ADT that decreased Bax expression in this region. In the CeA, again in direct contrast to the stress effects, exposure to all classes of ADTs significantly increased Bcl-2 mRNA. The selective regulation of Bcl-xl and Bax in hippocampal subfields and of Bcl-2 in the Cg cortex, amygdala, and hypothalamus suggests that these cellular adaptations contribute to the long-term neural plastic adaptations to stress and ADTs in cortical, hypothalamic, and limbic brain structures.

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Section: Introductionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Repeated Unpredictable Stress and Antidepressants Differentially Regulate Expression of the Bcl-2 Family of Apoptotic Genes in Rat Cortical, Hippocampal, and Limbic Brain Structures

Kosten

Galloway

Duman

et al. 2007

Neuropsychopharmacol

147

View full text Add to dashboard Cite

show abstract

“…Alternatively, Pizzagalli and colleagues 32 did not find any morphometric differences in the subgenual ACC in melancholic as well as in nonmelancholic depression subjects relative to healthy control subjects, but did find a reduced resting-state metabolism and increased delta activity only in patients with melancholic depression. Whereas some studies on amygdala volume in MDD patients revealed glial cell and volume reductions, 33,34 Frodl and colleagues 35 demonstrated an increased amygdala volume in patients with a first depressive episode in comparison with patients with recurrent MDD and healthy control subjects, as well as no differences between the latter 2 groups.…”

Section: Discussionmentioning

confidence: 98%

Enhanced rostral anterior cingulate cortex activation during cognitive control is related to orbitofrontal volume reduction in unipolar depression

Wagner

Koch

Schachtzabel

et al. 2008

Journal of Affective Disorders

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“…2). We refer the reader to original publications (Fitting et al, 2008;Grady et al, 2003;Hamidi et al, 2004;Palackal et al, 1993) for detailed descriptions. Briefly, neurons are darkly stained and make up a single large nucleolus.…”

Section: Stereological Analysesmentioning

confidence: 99%

Postnatal development of the amygdala: A stereological study in rats

Chareyron

Lavenex

2012

J of Comparative Neurology

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The amygdala is the central component of a functional brain system regulating fear and emotional behaviors. Studies of the ontogeny of fear behaviors reveal the emergence of distinct fear responses at different postnatal ages. Here, we performed a stereological analysis of the rat amygdala to characterize the cellular changes underlying its normal structural development. Distinct amygdala nuclei exhibited different patterns of postnatal development, which were largely similar to those we have previously shown in monkeys. The combined volume of the lateral, basal, and accessory basal nuclei increased by 113% from 1 to 3 weeks of age and by an additional 33% by 7 months of age. The volume of the central nucleus increased only 37% from 1 to 2 weeks of age and 38% from 2 weeks to 7 months. At 1 week of age, the medial nucleus was 77% of the 7-monthold's volume and exhibited a constant, marginal increase until 7 months. Neuron number did not differ in the amygdala from 1 week to 7 months of age. In contrast, astrocyte number decreased from 3 weeks to 2 months of age in the whole amygdala. Oligodendrocyte number increased in all amygdala nuclei from 3 weeks to 7 months of age. Our findings revealed that distinct amygdala nuclei exhibit different developmental profiles and that the rat amygdala is not fully mature for an extended period postnatally. We identified different periods of postnatal development of distinct amygdala nuclei and cellular components, which are concomitant with the ontogeny of different fear and emotional behaviors.

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Glial reduction in amygdala in major depressive disorder is due to oligodendrocytes

Cited by 324 publications

References 56 publications

Repeated Unpredictable Stress and Antidepressants Differentially Regulate Expression of the Bcl-2 Family of Apoptotic Genes in Rat Cortical, Hippocampal, and Limbic Brain Structures

Repeated Unpredictable Stress and Antidepressants Differentially Regulate Expression of the Bcl-2 Family of Apoptotic Genes in Rat Cortical, Hippocampal, and Limbic Brain Structures

Enhanced rostral anterior cingulate cortex activation during cognitive control is related to orbitofrontal volume reduction in unipolar depression

Postnatal development of the amygdala: A stereological study in rats

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