Neuronal cytoskeletal alterations in an experimental model of depression

Reinés, Analı́a; Cereseto, Marina; Ferrero, Alejandro; Bonavita, Carla D; Wikinski, Silvia

doi:10.1016/j.neuroscience.2004.08.026

Cited by 44 publications

(31 citation statements)

References 35 publications

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“…The LH paradigm was performed as previously described (Reinés et al, 2004) according to Nakagawa et al (1999) and Vollmayr and Henn (2001) with modifications. Rats were randomly assigned to LH or control (C) groups.…”

Section: Lh Paradigm In Ratsmentioning

confidence: 99%

“…Quantification of escape deficit, which allowed the identification of animals that displayed the despaired behavior, was performed as previously described (Reinés et al, 2004) according to Nakagawa et al (1999) and Vollmayr and Henn (2001) with modifications. Briefly, both LH and control animals were subjected to an avoidance task in a shuttle box which consisted of two equal-sized compartments divided by a Plexiglas partition fitted out with an opening (7 Â 7 cm) and with a grid floor consisting of stainless-steel rods placed 1-cm apart.…”

Section: Lh Paradigm In Ratsmentioning

confidence: 99%

“…Similarly as reported elsewhere (Reinés et al, 2004;Ferrero et al, 2007), 1 h after the corresponding LH test session, animals were deeply anesthetized (50 mg/kg ketamine hydrochloride and 2 mg/kg xylazine, i.p.) and perfused through the left ventricle with 4% paraformaldehyde.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…Brain sections were processed in freefloating state as previously described (Reinés et al, 2004). After inhibition of endogenous peroxidase activity, brain sections were blocked with 3% v/v normal ovine serum and incubated for 48 h at 41C with one of the following primary monoclonal antibodies against NFL, NFM, NFH, or MAP-2, diluted 1 : 1000 and 1 : 2000 v/v for NFs and MAP-2, respectively.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…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%

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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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Section: Lh Paradigm In Ratsmentioning

confidence: 99%

Section: Lh Paradigm In Ratsmentioning

confidence: 99%

Section: Immunohistochemistrymentioning

confidence: 99%

Section: Immunohistochemistrymentioning

confidence: 99%

Section: Morphometric Measurementmentioning

confidence: 99%

See 3 more Smart Citations

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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Specific neuronal subpopulations in the rat basolateral amygdala express high levels of nonphosphorylated neurofilaments

McDonald

Mascagni

2021

J of Comparative Neurology

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Cortical pyramidal neurons (PNs) containing nonphosphorylated neurofilaments (NNFs) localized with the SMI‐32 monoclonal antibody have been shown to be especially vulnerable to degeneration in Alzheimer's disease (AD). The present investigation is the first to study the expression of SMI‐32+ NNFs in neurons of the basolateral nuclear complex of the amygdala (BNC), which contains cortex‐like PNs and nonpyramidal neurons (NPNs). We observed that PNs in the rat basolateral nucleus (BL), but not in the lateral (LAT) or basomedial (BM) nuclei, have significant levels of SMI‐32‐ir in their somata with antibody diluents that did not contain Triton X‐100, but staining in these cells was greatly attenuated when the antibody diluent contained 0.3% Triton. Using Triton‐containing diluents, we found that all SMI‐32+ neurons in all three of the BNC nuclei were NPNs. Using a dual‐labeling immunoperoxidase technique, we demonstrated that most of these SMI‐32+ NPNs were parvalbumin‐positive (PV+) or somatostatin‐positive NPNs but not vasoactive intestinal peptide‐positive or neuropeptide Y‐positive NPNs. Using a technique that combines retrograde tracing with SMI‐32 immunohistochemistry using intermediate levels of Triton in the diluent, we found that all BNC neurons projecting to the mediodorsal thalamic nucleus (MD) were large NPNs, and most were SMI‐32+. In contrast, BNC neurons projecting to the ventral striatum or cerebral cortex were PNs that expressed low levels of SMI‐32 immunoreactivity (SMI‐32‐ir) in the BL, and no SMI‐32‐ir in the LAT or BM. These data suggest that the main neuronal subpopulations in the BNC that degenerate in AD may be PV+ and MD‐projecting NPNs.

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Maternal exposure to 3,3’‐iminodipropionitrile targets late‐stage differentiation of hippocampal granule cell lineages to affect brain‐derived neurotrophic factor signaling and interneuron subpopulations in rat offspring

Itahashi

Abe

Tanaka

et al. 2014

J of Applied Toxicology

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3,3'-Iminodipropionitrile (IDPN) causes neurofilament (NF)-filled swellings in the proximal segments of many large-caliber myelinated axons. This study investigated the effect of maternal exposure to IDPN on hippocampal neurogenesis in rat offspring using pregnant rats supplemented with 0 (controls), 67 or 200 ppm IDPN in drinking water from gestational day 6 to day 21 after delivery. On postnatal day (PND) 21, female offspring subjected to analysis had decreased parvalbumin(+), reelin(+) and phospho-TrkB(+) interneurons in the dentate hilus at 200 ppm and increased granule cell populations expressing immediate-early gene products, Arc or c-Fos, at ≥ 67 ppm. mRNA expression in the dentate gyrus examined at 200 ppm decreased with brain-derived neurotrophic factor (Bdnf) and very low density lipoprotein receptor. Immunoreactivity for phosphorylated NF heavy polypeptide decreased in the molecular layer of the dentate gyrus and the stratum radiatum of the cornu ammonis (CA) 3, portions showing axonal projections from mossy cells and pyramidal neurons, at 200 ppm on PND 21, whereas immunoreactivity for synaptophysin was unchanged in the dentate gyrus. Observed changes all disappeared on PND 77. There were no fluctuations in the numbers of apoptotic cells, proliferating cells and subpopulations of granule cell lineage in the subgranular zone on PND 21 and PND 77. Thus, maternal IDPN exposure may reversibly affect late-stage differentiation of granule cell lineages involving neuronal plasticity as evident by immediate-early gene responses to cause BDNF downregulation resulting in a reduction in parvalbumin(+) or reelin(+) interneurons and suppression of axonal plasticity in the mossy cells and CA3 pyramidal neurons.

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Neuronal cytoskeletal alterations in an experimental model of depression

Cited by 44 publications

References 35 publications

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

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

Specific neuronal subpopulations in the rat basolateral amygdala express high levels of nonphosphorylated neurofilaments

Maternal exposure to 3,3’‐iminodipropionitrile targets late‐stage differentiation of hippocampal granule cell lineages to affect brain‐derived neurotrophic factor signaling and interneuron subpopulations in rat offspring

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