Chronic psychosocial stress does not affect the number of pyramidal neurons in tree shrew hippocampus

Vollmann-Honsdorf, Gesa K; Flügge, Gabriele; Fuchs, Eberhard

doi:10.1016/s0304-3940(97)00647-2

Cited by 93 publications

(47 citation statements)

References 17 publications

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“…Massive neuronal loss following exposure to repeated episodes of hypercortisolemia can be excluded, because, in human post-mortem brain tissue of severely depressed patients or of steroid hormone treated human or nonhuman primate subjects, no major cell loss was apparent, nor was any neuropathology present (Leverenz et al, 1999;Lucassen et al, 2001;Müller et al, 2001;Stockmeier et al, 2004). This is consistent with findings of preclinical studies that failed to reveal any loss of principal neurons in the hippocampal formation after chronic stress exposure (Vollmann-Honsdorf et al, 1997;Sousa et al, 1998;Keuker et al, 2001). Stress-induced dendritic retraction of CA3 pyramidal neurons and suppression of dentate neurogenesis have been implicated as mechanisms contributing to hippocampal shrinkage (McEwen, 2000).…”

Section: Morphological Changes Of Astroglia May Contribute To Hippocasupporting

confidence: 74%

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

Czéh

Simon

Schmelting

et al. 2005

Neuropsychopharmacol

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408

252

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Analysis of post-mortem tissue from patients with affective disorders has revealed a decreased number of glial cells in several brain areas. Here, we examined whether long-term psychosocial stress influences the number and morphology of hippocampal astrocytes in an animal model with high validity for research on the pathophysiology of major depression. Adult male tree shrews were submitted to 5 weeks of psychosocial stress, after which immunocytochemical and quantitative stereological techniques were used to estimate the total number and somal volume of glial fibrillary acidic protein-positive astrocytes in the hippocampal formation. Stress significantly decreased both the number (À25%) and somal volume (À25%) of astroglia, effects that correlated notably with the stress-induced hippocampal volume reduction. Additionally, we examined whether antidepressant treatment with fluoxetine, a selective serotonin reuptake inhibitor, offered protection from these stress-induced effects. Animals were subjected to 7 days of psychosocial stress before the onset of daily oral administration of fluoxetine (15 mg/kg per day), with stress continued throughout the 28-day treatment period. Fluoxetine treatment prevented the stress-induced numerical decrease of astrocytes, but had no counteracting effect on somal volume shrinkage. In nonstressed animals, fluoxetine treatment had no effect on the number of astrocytes, but stress exposure significantly reduced their somal volumes (À20%). These notable changes of astroglial structural plasticity in response to stress and antidepressant treatment support the notion that glial changes may contribute to the pathophysiology of affective disorders as well as to the cellular actions of antidepressants.

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Section: Morphological Changes Of Astroglia May Contribute To Hippocasupporting

confidence: 74%

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

Czéh

Simon

Schmelting

et al. 2005

Neuropsychopharmacol

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408

252

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“…By using in vivo imaging with magnetic resonance spectroscopy, the present study showed that psychosocial stress caused a reduction in the neuroaxonal marker NAA and that this change could be prevented by tianeptine treatment, providing a neurochemical endpoint for antidepressant treatments in vivo. Previously, in the tree shrew model, we could demonstrate a mild stress-induced hippocampal volume loss in vivo by magnetic resonance imaging (62), and we found that this loss is due neither to reduction in neuron number nor to increased apoptotic cells in the Ammon's horn (63,64).…”

Section: Stress-induced Reduction In Cell Proliferation Is Prevented mentioning

confidence: 66%

Stress-induced changes in cerebral metabolites, hippocampal volume, and cell proliferation are prevented by antidepressant treatment with tianeptine

Czéh

Michaelis

Watanabe

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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969

611

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Stress-induced structural remodeling in the adult hippocampus, involving debranching and shortening of dendrites and suppression of neurogenesis, provides a cellular basis for understanding the impairment of neural plasticity in the human hippocampus in depressive illness. Accordingly, reversal of structural remodeling may be a desirable goal for antidepressant therapy. The present study investigated the effect of tianeptine, a modified tricyclic antidepressant, in the chronic psychosocial stress model of adult male tree shrews (Tupaia belangeri), a model with high validity for research on the pathophysiology of major depression. Animals were subjected to a 7-day period of psychosocial stress to elicit stress-induced endocrine and central nervous alterations before the onset of daily oral administration of tianeptine (50 mg͞kg). The psychosocial stress continued throughout the treatment period of 28 days. Brain metabolite concentrations were determined in vivo by proton magnetic resonance spectroscopy, cell proliferation in the dentate gyrus was quantified by using BrdUrd immunohistochemistry, and hippocampal volume was measured post mortem. Chronic psychosocial stress significantly decreased in vivo concentrations of N-acetyl-aspartate (؊13%), creatine and phosphocreatine (؊15%), and choline-containing compounds (؊13%). The proliferation rate of the granule precursor cells in the dentate gyrus was reduced (؊33%). These stress effects were prevented by the simultaneous administration of tianeptine yielding normal values. In stressed animals treated with tianeptine, hippocampal volume increased above the small decrease produced by stress alone. These findings provide a cellular and neurochemical basis for evaluating antidepressant treatments with regard to possible reversal of structural changes in brain that have been reported in depressive disorders.neurogenesis ͉ proton magnetic resonance spectroscopy ͉ depression ͉ hippocampus ͉ tree shrew D epressive disorders are among the most common and lifethreatening illnesses and represent a significant public health problem (1). Despite extensive preclinical and clinical investigations, the exact neurobiological processes leading to depression and the mechanisms responsible for the therapeutic effects of antidepressant drugs are not completely understood (2).The hippocampus is one of the brain structures that has been extensively studied with regard to the actions of stress, depression and antidepressant actions (3, 4). Recent imaging studies in humans revealed that the hippocampus undergoes selective volume reduction in stress-related neuropsychiatric disorders such as recurrent depressive illness (5-7). Within the hippocampal formation, the dentate gyrus is one of the few brain structures where production of new neurons occurs even in the adult mammalian brain (8-10). Several experiential, neuroendocrine, and genetic factors that regulate neurogenesis in the adult dentate gyrus have been identified (11). One factor that potently suppresses adult granule cell prolife...

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“…However, by stereological analyses, long-term psychosocial stress in tree shrews did not affect the numbers of neurons in the hippocampus [57], nor were hippocampal neuron numbers influences by chronic, stress-like levels of exogenous glucocorticoids in aged macaques [27]. Unfortunately, no individual data on cortisol levels or cognitive state exist for the human subjects, whose hippocampi had been stereologically investigated [55,63].…”

Section: Discussionmentioning

confidence: 99%

Preservation of hippocampal neuron numbers in aged rhesus monkeys

Keuker

Luiten

Fuchs

2003

Neurobiology of Aging

123

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Preservation of hippocampal neuron numbers in aged rhesus monkeys Keuker, J.I.H.; Luiten, P.G.M.; Fuchs, E. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. AbstractTo investigate whether or not aging of nonhuman primates is accompanied by a region-specific neuron loss in the hippocampal formation, we used the optical fractionator technique to obtain stereological estimates of unilateral neuron numbers of the hippocampi of eight young (0-4 years) and five aged (18-31 years) male rhesus monkeys (Macaca mulatta). Our results show a preservation of neurons (mean × 10 3 ± S.D. × 10 3 ) in the subiculum (young = 588 ± 124, aged = 612 ± 207), CA1 (young = 1051 ± 249, aged = 1318 ± 311), CA2 (young = 100 ± 18, aged = 113 ± 12), CA3 (young = 478 ± 125, aged = 509 ± 139), hilus (young = 337 ± 115, aged = 394 ± 90), and dentate gyrus (young = 5550 ± 1725, aged = 7799 ± 2087) of the hippocampal formation. These results confirm a previous stereological study in rhesus monkeys, but are in conflict with data for humans, showing age-dependent region-specific alterations in the hippocampal formation.

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Chronic psychosocial stress does not affect the number of pyramidal neurons in tree shrew hippocampus

Cited by 93 publications

References 17 publications

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

Stress-induced changes in cerebral metabolites, hippocampal volume, and cell proliferation are prevented by antidepressant treatment with tianeptine

Preservation of hippocampal neuron numbers in aged rhesus monkeys

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