2015
DOI: 10.1016/j.yhbeh.2015.01.010
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Exposure to social defeat stress in adolescence improves the working memory and anxiety-like behavior of adult female rats with intrauterine growth restriction, independently of hippocampal neurogenesis

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Cited by 9 publications
(5 citation statements)
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“…We have previously shown that cell proliferation (Ki67+) in the subventricular zone is increased in IUGR fetal guinea pigs (Tolcos et al (2015), and others report that ischemia in adult rats increases neurogenesis (Jin et al, 2001; Jin et al, 2003), consistent with the findings in the current study. In a model of IUGR induced by systemic exposure to thromboxane A2, increased cell proliferation (Brd‐U labeled cells), but not differentiation (Brd‐U/NeuN colabeled cells) in rats during adulthood (Furuta et al, 2015) suggest that newly generated cells may not continue into subsequent phases of neurogenesis, however our results suggest the contrary, at least in adolescence. Alternatively, the observed increase in DCX+ linear density may have occurred as a result of an increased sensitivity to learning‐modulated neurogenesis, as previously reported for adult‐generated neurons in the DG (Gould, Beylin, Tanapat, Reeves, & Shors, 1999; Leuner et al, 2004).…”
Section: Discussioncontrasting
confidence: 52%
“…We have previously shown that cell proliferation (Ki67+) in the subventricular zone is increased in IUGR fetal guinea pigs (Tolcos et al (2015), and others report that ischemia in adult rats increases neurogenesis (Jin et al, 2001; Jin et al, 2003), consistent with the findings in the current study. In a model of IUGR induced by systemic exposure to thromboxane A2, increased cell proliferation (Brd‐U labeled cells), but not differentiation (Brd‐U/NeuN colabeled cells) in rats during adulthood (Furuta et al, 2015) suggest that newly generated cells may not continue into subsequent phases of neurogenesis, however our results suggest the contrary, at least in adolescence. Alternatively, the observed increase in DCX+ linear density may have occurred as a result of an increased sensitivity to learning‐modulated neurogenesis, as previously reported for adult‐generated neurons in the DG (Gould, Beylin, Tanapat, Reeves, & Shors, 1999; Leuner et al, 2004).…”
Section: Discussioncontrasting
confidence: 52%
“…= [214] ↓4-23% [79,87,88,[93][94][95][96] = [201,215] ↓7-52% [91,92,[97][98][99][100][101]216] ↓9.5-14% [83,89] = [84] ↓[128, 129,131,146] ↓8-40% [99,112,114,115,160,203,217,218] ↓36-42% [145,162] ↓18-44% [102, 116-118, 163, 212] ↓42-48% [122,124,125] ↓17-28% [132,[134][135][136][137][138][139][140][141] Brain size = [214] ↓cerebrum, 11% [79] ↓11-66% [90,…”
Section: Birth Weightmentioning
confidence: 99%
“…Corpus callosum ↓ [115] ↓width [162] NEURONAL DENSITY Cerebrum = [79] ↓insular, temporal and occipital cortex, indirect evidence [117] Hippocampus = [85] ↑ neuronal proliferation, adolescent females [131] = [113,115] ↑degenerating neurons, CA3 [113] ↓indirect evidence [117] Dentate gyrus = [101] Cerebellum = [79] ↓ indirect evidence via MRI [117] Fornix ↑ degenerating neurons [113] Entorhinal cortex ↓ [113,115] ↑ degenerating neurons [113] Cingulate cortex = [113] External capsule ↑ degenerating neurons [113] Prefrontal cortex = [115] ↓ indirect evidence [117] GABAergic interneurons ↑ prefrontal cortex [115] …”
Section: ↓[162]mentioning
confidence: 99%
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“…Finally, working memory performances in social defeated animals varied, in delay- and species-dependent manners. In the T-maze alternation task, mice displayed a decrease in alternation rate as soon as the 5-seconds delay [ 146 ] whereas the alternation rate was not affected in rats, neither at 10 or 30 or 60 s delays [ 147 , 148 ]. The delay must rise to 90 s to induce a deficit in working memory in adult defeated-rats compared to controls [ 147 ].…”
Section: Working Memory Deficits In Rodent Models Of Anxiety/deprementioning
confidence: 99%