Neuroglial interactions in a model of para-chlorophenylalanine-induced serotonin depletion

Ramos, Alberto Javier; Tagliaferro, Patricia; López, Ester Marı́a; Saavedra, Jorge Pecci; Brusco, Alicia

doi:10.1016/s0006-8993(00)02862-6

Cited by 41 publications

(35 citation statements)

References 47 publications

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“…The serotonin reduction might be impairing S100B release from the astrocyte, with the concomitant intracellular accumulation and decreased extracellular S100B levels, thus diminishing its neurotrophic effects. In fact, in a model of induction of serotonin depletion, we have demonstrated astroglial reaction both in the serotoninergic nucleus and in their innervation areas (Tagliaferro et al, 1997) as well as an increased astrocytic intracellular expression of S100B protein with changes in neuronal processes morphology (Ramos et al, 2000). The increased immunoreactivity in astrocytes observed in this study might be related to an elevated production of S100B and/or a cytoplasmatic accumulation resulting from reduced release.…”

Section: Astrocyte-neuron Changes In Prenatal Stresssupporting

confidence: 55%

“…As previously described (Tagliaferro et al, 1997;Ramos et al, 2000), ROD was obtained after the transformation of mean gray values into ROD by using the formula: ROD ¼ log(256/mean gray). A background parameter was obtained from each section out of the immunolabelled cells and subtracted from each cell before statistically processing the obtained values.…”

Section: Image Analysis Morphometric Studiesmentioning

confidence: 99%

“…The morphometric studies using immunolabelled structures for cytoskeletal proteins were performed as previously described (Ramos et al, 2000). To evaluate the MAP-2-IR fibers, the total area of the immunolabelled fibers was related to the total area of the corresponding microscopic field, thus rendering a relative area parameter.…”

Section: Image Analysis Morphometric Studiesmentioning

confidence: 99%

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Astrocyte–neuron vulnerability to prenatal stress in the adult rat brain

Barros

Vega

Caltana

et al. 2006

J of Neuroscience Research

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Chronic activation of the stress response during pregnancy has been shown to be injurious to the development of the offspring. We have previously demonstrated that restraint prenatal stress inflicted during the last week of pregnancy in rats increased dopamine and glutamate receptors in forebrain areas of the adult offsprings. In this study, the same prenatal insult was employed to assess morphological changes in astrocytes and in the dendritic arborization in frontal cortex, striatum, and hippocampus of the adult rat brain. On postnatal day 90, brains were processed for immunocytochemistry using primary antibodies to glial fibrillary acidic protein (GFAP; the main cytoskeletal astroglial protein), S100B protein (an astroglial-derived neurotrophic factor), MAP-2 (a microtubule-associated protein present almost exclusively in dendrites), and synaptophysin (Syn; one major integral protein of the synaptic vesicles membrane). The results show a significant increase in the cell area of GFAP-immunoreactive (-IR) astrocytes, with high levels of S100B protein and a significant decrease in the relative area of MAP-2-IR neuronal processes in prenatally stressed adult rats. The expression of synaptophysin decreased in all areas studied. These results demonstrate that prenatal stress induces a long-lasting astroglial reaction and a reduced dendritic arborization, with synaptic loss in the brain of adult offspring. In addition to the neurochemical alterations previously reported, these morphological changes might be underlying the behavioral and learning impairment previously observed in prenatally stressed rats.

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Section: Astrocyte-neuron Changes In Prenatal Stresssupporting

confidence: 55%

Section: Image Analysis Morphometric Studiesmentioning

confidence: 99%

Section: Image Analysis Morphometric Studiesmentioning

confidence: 99%

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Astrocyte–neuron vulnerability to prenatal stress in the adult rat brain

Barros

Vega

Caltana

et al. 2006

J of Neuroscience Research

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“…Brain sections of animals belonging to the different experimental groups were simultaneously processed in the freefloating state as previously described (Ramos et al, 2000(Ramos et al, , 2004. Briefly, sections to be used for light microscopy were dehydrated, and endogenous peroxidase activity was inhibited with 0.5% v/v H 2 O 2 in methanol for 30 min at room temperature.…”

Section: Immunohistochemistrymentioning

confidence: 99%

p75^NTR Expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization

Angelo

Aviles-Reyes

Villarreal

et al. 2009

J of Neuroscience Research

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The p75 neurotrophin receptor (p75(NTR)) is involved in neuronal functions ranging from induction of apoptosis and growth inhibition to the promotion of survival. p75(NTR) expression is induced in the central nervous system (CNS) by a range of pathological conditions, where it seems to have a role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75(NTR) expression in cell lines and primary neurons is Sp1 dependent (Ramos et al. [2007] J. Neurosci. 27:1498). In this study, we analyzed the spatiotemporal profile of p75(NTR) expression after an ischemic lesion induced by cortical devascularization (CD). Our results show that p75(NTR) expression occurs in isolated neurons of the ischemic lesion site. The p75(NTR+) neurons presented morphological alterations and active caspase-3 staining. Some p75(NTR+) neurons were also positive for sortilin. The peak of p75(NTR) expression was localized 3 days postlesion (3DPL) in the penumbra. Sp1 transcription factor nuclear localization was observed in p75(NTR+) neurons. The overall level of Sp1 expression was increased until 14DPL on the ipsilateral hemisphere. With primary cortical neurons, we demonstrated that p75(NTR) expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75(NTR) expression is localized in selected neurons of the ischemic lesion and that these neurons are probably condemned to apoptotic cell death. In primary neuronal culture, it is clear that excitotoxicity and Sp1 are involved in induction of p75(NTR) expression, although, in vivo, some additional mechanisms are likely to be involved in the control of p75(NTR) expression in specific neurons in vivo.

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“…The resolution of each pixel was 256 gray levels. Threshold setting was performed according to previous reports (Ramos et al, 2000;Tagliaferro et al, 2002;Reinés et al, 2004). For that purpose, a range of gray value (threshold value) was interactively selected to allow the segmentation of the specific signal from the background and thereafter was kept constant along each experiment.…”

Section: Morphometric Measurementmentioning

confidence: 99%

Maintenance Treatment with Fluoxetine is Necessary to Sustain Normal Levels of Synaptic Markers in an Experimental Model of Depression: Correlation with Behavioral Response

Reinés

Cereseto

Ferrero

et al. 2007

Neuropsychopharmacol

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Dysfunction of hippocampal plasticity has been proposed to play a critical role in the pathophysiology of depression. However, antidepressant drug effects on synaptic plasticity and cytoskeletal remodeling remain controversial. The aim of the present study was to evaluate in animals exposed to the learned helplessness (LH) paradigm, an accepted experimental model of depression, the effect of chronic treatment with fluoxetine (FLX) on synaptic and cytoskeletal proteins known to undergo plastic changes. Synaptophysin (SYN), postsynaptic density 95 (PSD-95), axon growth-associated protein 43 (GAP-43), and cytoskeletal proteins (intermediate neurofilaments and MAP-2) were studied in the hippocampus by immunohistochemistry. Whereas LH animals treated 21 days with saline (LH-S group) displayed diminished SYN and PSD-95 immunostainings in the CA3 but not in the DG, chronic treatment with FLX not only reversed the despaired behavior induced by exposure to LH paradigm, but also fully recovered SYN and PSD-95 labeling to control values. Similar results were obtained for the axonal remodeling marker GAP-43. FLX treatment did not modify either the decreased light neurofilament subunit (NFL) observed in the hippocampus of LH animals or any other cytoskeletal protein studied. When FLX treatment was withdrawn for 90 days in those LH-FLX animals in which reversion of despair had been observed at day 25, recurrence of despaired behavior was found accompanied by decreased SYN, PSD-95, and NFL labelings. Results indicate that the synapse remodeling induced by FLX in the CA3 region could underlie its behavioral efficacy despite the absence of cytoskeletal remodeling and that the stability of synaptic changes would depend on the continuous administration of the drug.

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Neuroglial interactions in a model of para-chlorophenylalanine-induced serotonin depletion

Cited by 41 publications

References 47 publications

Astrocyte–neuron vulnerability to prenatal stress in the adult rat brain

Astrocyte–neuron vulnerability to prenatal stress in the adult rat brain

p75^NTR Expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization

Maintenance Treatment with Fluoxetine is Necessary to Sustain Normal Levels of Synaptic Markers in an Experimental Model of Depression: Correlation with Behavioral Response

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Neuroglial interactions in a model of para-chlorophenylalanine-induced serotonin depletion

Cited by 41 publications

References 47 publications

Astrocyte–neuron vulnerability to prenatal stress in the adult rat brain

Astrocyte–neuron vulnerability to prenatal stress in the adult rat brain

p75NTR Expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization

Maintenance Treatment with Fluoxetine is Necessary to Sustain Normal Levels of Synaptic Markers in an Experimental Model of Depression: Correlation with Behavioral Response

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p75^NTR Expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization