Acute Stress in Pregnant RatsEffects on Growth Rate, Learning, and Memory Capabilities of the Offspring

Lordi, B; Protais, P.; Mellier, Daniel; Caston, J.

doi:10.1016/s0031-9384(97)00261-8

Cited by 75 publications

(39 citation statements)

References 26 publications

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“…This observation was recently extended by Nishio et al (2001) who reported that rats, prenatally stressed using a sound stress, exhibit an increased in total number of errors in the water-maze and time spent searching for the platform location. Lordi et al (1997) also previously described that adult PS rats are impaired for delayed alternation behavior, with an ITI of 1 h but not with an ITI of 30 s or 3 min, and in a passive avoidance response. Finally, PS rats show an enhancement of the age (16-22 month)-related recognition memory impairment in a Y-maze procedure and the age-related working memory impairment in the radial-arm maze, as compared to nonstressed offspring rats (Valle´e et al, 1999).…”

Section: Discussionmentioning

confidence: 74%

“…Consequently, PS offspring exhibits elevated neuroendocrine responses to stress, including elevated secretions of corticotropin-releasing factor (CRF), adrenocorticotropin-releasing hormone (ACTH) and corticosterone (Peters, 1982;Maccari et al, 1995;Weinstock et al, 1998), and a reduction in the density of corticosteroid receptors in the hippocampus (Weinstock, 1997;Valle´e et al, 1999). Finally, the hippocampus appears as a brain structure sensitive to PS (Weinstock, 1997;Valle´e et al, 1999) and PS offspring shows from infancy to senescence and throughout adulthood marked memory deficits in numerous, and particularly hippocampal-dependent, behavioral tasks (Szuran et al, 1994;Lordi et al, 1997;Valle´e et al, 1999). We previously reported that a maternal restraint stress, administered during the last week of gestation, results in marked learning and memory impairments in 4-week-old offspring rats (Gue´et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Meunier

Gué

Récasens

et al. 2004

British J Pharmacology

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1 Stress during pregnancy results in complex neurochemical and behavioral alterations throughout the offspring lifetime. We here examined the impact of prenatal stress (PS) on memory functions in male and female offspring and report the efficacy of a selective sigma 1 (s 1 ) receptor agonist, igmesine, in alleviating the observed deficits. 2 Dams received an unpredictable 90-min duration restraint stress from gestational day E17 to E20. Learning was examined in offspring between day P24 and P36 using spontaneous alternation in the Y-maze, delayed alternation in the T-maze, water-maze learning and passive avoidance. 3 Both male and female PS rats showed impairments of spontaneous and delayed alternation performances. Acquisition of a fixed platform position in the water-maze was unchanged in PS rats, but the probe test revealed a diminution of time spent in the training quadrant. Acquisition of a daily changing platform position demonstrated impaired working memory for male and female PS rats. Finally, passive avoidance deficits were observed. 4 Pretreatment with the selective s 1 agonist igmesine (1-10 mg kg À1 i.p.) reversed the PS-induced learning deficits in offspring rats for each test. The s 1 antagonist BD1063 failed to affect performances alone but blocked the igmesine effect, confirming the involvement of the s 1 receptor. 5 PS thus induces delayed memory deficits, affecting spatial and nonspatial, short-and long-term memories in juvenile male and female offspring rats. Activation of the s 1 neuromodulatory receptor allows a significant recovery of the memory functions in PS rats.

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Meunier

Gué

Récasens

et al. 2004

British J Pharmacology

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“…This finding is of particular interest because the dentate gyrus is associated with spatial learning and memory (35,36), which clearly are affected in prenatally stressed rats (present data and refs. 2,4,5).…”

Section: Discussionmentioning

confidence: 99%

“…Deleterious life events during pregnancy induce neurobiological and behavioral defects in offspring, some of them involving the hippocampal formation (1)(2)(3)(4)(5). Indeed, prenatal stress results in an enhanced production of stress hormones by the mother during critical periods of fetal brain development and provokes a definitively longer corticosterone response to stress in the offspring associated with a reduction in the number of hippocampal corticosteroid receptors (1,3,5).…”

mentioning

confidence: 99%

“…Indeed, prenatal stress results in an enhanced production of stress hormones by the mother during critical periods of fetal brain development and provokes a definitively longer corticosterone response to stress in the offspring associated with a reduction in the number of hippocampal corticosteroid receptors (1,3,5). Behaviorally, the progeny, from adulthood to senescence, exhibit memory deficits in a hippocampal-dependent task (2,4,5).…”

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confidence: 99%

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Prenatal stress produces learning deficits associated with an inhibition of neurogenesis in the hippocampus

Lemaire

Koehl

Moal

et al. 2000

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

928

637

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Early experiences such as prenatal stress significantly influence the development of the brain and the organization of behavior. In particular, prenatal stress impairs memory processes but the mechanism for this effect is not known. Hippocampal granule neurons are generated throughout life and are involved in hippocampaldependent learning. Here, we report that prenatal stress in rats induced lifespan reduction of neurogenesis in the dentate gyrus and produced impairment in hippocampal-related spatial tasks. Prenatal stress blocked the increase of learning-induced neurogenesis. These data strengthen pathophysiological hypotheses that propose an early neurodevelopmental origin for psychopathological vulnerabilities in aging. It is well documented from animal studies that during the perinatal period, the development of an organism is subjected to complex environmental influences. Deleterious life events during pregnancy induce neurobiological and behavioral defects in offspring, some of them involving the hippocampal formation (1-5). Indeed, prenatal stress results in an enhanced production of stress hormones by the mother during critical periods of fetal brain development and provokes a definitively longer corticosterone response to stress in the offspring associated with a reduction in the number of hippocampal corticosteroid receptors (1,3,5). Behaviorally, the progeny, from adulthood to senescence, exhibit memory deficits in a hippocampal-dependent task (2, 4, 5).Recently, it has been hypothesized that hippocampal-mediated learning (6) may be related to the generation of new neurons in the adult dentate gyrus (7,8,9). These newborn cells migrate in the granule cell layer, and differentiate in granule neurons whose projections, the mossy fibers, extend to the CA3 hippocampal region (10, 11). Furthermore, the size of the mossy fibers' projections correlates with variations in performances in spatial memory tests (12, 13). Finally, glucocorticoid levels regulate de novo cell proliferation in the dentate gyrus. Indeed, adrenalectomy performed in young or aged rats increases neurogenesis, an effect that is prevented by glucocorticoid treatment (14,15,16). These results raised the critical question as to whether prenatal stress can impair neurogenesis and, if so, whether it is related to learning ability.To test this hypothesis, we first examined cell proliferation in the progeny of stressed mothers with 5-bromo-2Ј-deoxyuridine (BrdUrd), a thymidine analogue incorporated into genetic material during synthetic DNA phase (S phase) of mitotic division. Cellspecific markers were used to phenotype the newly born neurons after longer survival times. We next examined whether the structural hippocampal defects resulting from prenatal stress had functional consequences on learning abilities. Finally, we examined whether the reduction in cell proliferation in the dentate gyrus had an impact on spatial memory, a hypothesis supported by others (17). MethodsHousing Conditions. Adult virgin Sprague-Dawley female rats (Iffa Credo) ...

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Biological Effects of Long-Duration, High-Field (4 T) MRI on Growth and Development in the Mouse

Magin

Lee

Klintsova

et al. 2000

J. Magn. Reson. Imaging

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The effects of long-duration, high-field magnetic resonance imaging (MRI) on fetal growth and postnatal development in mice were studied. Seven experimental groups of pregnant ICR mice were exposed for 9 hours on day 9 and/or day 12 post coitus (pc) to magnetic fields (4 T static, 5 T/sec switched gradient, and 0.2 W/kg radiofrequency at 170 MHz) associated with MRI conditions. Two experimental groups (sham and exposure groups) were exposed to a combination of ultrasound (day 9 pc, 3.25 MHz, focused) and MRI-associated fields (day 12 pc). No statistically significant changes in fetal growth were observed in the animals exposed to only MRI or ultrasound fields. However, in the combined ultrasound and MRI-exposed group, the fetal weight and crown-rump length were reduced compared with the sham and cage controls. These results suggest that MRI and ultrasound exposure well in excess of current clinical conditions can exert biological effects if applied at sensitive stages of fetal development.

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Acute Stress in Pregnant RatsEffects on Growth Rate, Learning, and Memory Capabilities of the Offspring

Cited by 75 publications

References 26 publications

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Prenatal stress produces learning deficits associated with an inhibition of neurogenesis in the hippocampus

Biological Effects of Long-Duration, High-Field (4 T) MRI on Growth and Development in the Mouse

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Acute Stress in Pregnant RatsEffects on Growth Rate, Learning, and Memory Capabilities of the Offspring

Cited by 75 publications

References 26 publications

Attenuation by a sigma1 (σ1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Attenuation by a sigma1 (σ1) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Prenatal stress produces learning deficits associated with an inhibition of neurogenesis in the hippocampus

Biological Effects of Long-Duration, High-Field (4 T) MRI on Growth and Development in the Mouse

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Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats

Attenuation by a sigma₁ (σ₁) receptor agonist of the learning and memory deficits induced by a prenatal restraint stress in juvenile rats