Reversal of cognitive deficit of apolipoprotein E knockout mice after repeated exposure to a common environmental experience

Grootendorst, Jeannette; Kloet, E. Ronald de; Dalm, Sergiu; Oitzl, Melly S.

doi:10.1016/s0306-4522(01)00412-2

Cited by 58 publications

(42 citation statements)

References 50 publications

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“…When age-matched apoE-deficient mice were compared with wild-type for these agesensitive aspects of cognitive performance, they showed markedly greater age-related impairments in initial learning of spatial discrimination, but did not differ from wild-type in any of the other dimensions of age-related cognitive decline that were tested. While the observation of accelerated deficits in spatial swim maze performance of apoE-deficient mice is consistent with previous literature (Gordon et al 1995(Gordon et al , 1996Masliah et al 1997;Oitzl et al 1997;Veinbergs et al 1999Veinbergs et al , 2000Grootendorst et al 2001), the current studies suggest that the accelerated decline does not extend to several other dimensions of learning and memory performance. Thus, brain processes targeted by apoE deficiency could be relatively selective when compared with those involved in normal brain aging.…”

Section: Discussionsupporting

confidence: 92%

Lifelong vitamin E intake retards age-associated decline of spatial learning ability in apoE-deficient mice

McDonald

Forster

2005

AGE

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The potential for lifelong vitamin E supplementation to delay age-associated cognitive decline was tested in apoE-deficient and wild-type C57BL/6 mice. Beginning at eight weeks of age, the mice were maintained on a control diet or diets supplemented with DL-a-tocopheryl acetate yielding approximate daily intakes of either 20 or 200 mg/kg body weight. When 6 or 18 months of age, cognitive functioning of the mice was assessed using swim maze and discriminated avoidance testing procedures. For the mice maintained on control diets, the agerelated declines in swim maze performance were relatively larger in apoE-deficient mice when compared with wild-type. On the other hand, age-associated declines in learning and working memory for discriminated avoidance were similar in the two genotypes. The 200-mg/kg dose of vitamin E prevented the accelerated decline in spatial learning apparent in 18-month-old apoE-deficient mice, but had no equivalent effect on performance declines attributable to normal aging in the wild-type mice. Vitamin E supplementation failed to prevent agerelated impairments in learning and memory for discriminated avoidance observed in both the wild-type and apoE-deficient mice. The current findings are consistent with the hypothesis that apoE deficiency confers an accelerated, though probably selective, loss of brain function with age. This loss of function would appear to involve pathogenic oxidative mechanisms that can be prevented or offset by antioxidant supplementation.

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Section: Discussionsupporting

confidence: 92%

Lifelong vitamin E intake retards age-associated decline of spatial learning ability in apoE-deficient mice

McDonald

Forster

2005

AGE

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“…Clearly, we cannot exclude that other changes in the GR (or MR) signaling pathways may underlie the observed dichotomy in cellular responses to CORT. Interestingly, such a dichotomy in responsivity to CORT has been described previously, where exposure to stress or CORT before training in the Morris water maze impaired learning in wild-type mice but facilitated learning in the apolipoproteinE knock-out mice (Grootendorst et al, 2001).…”

Section: Corticosterone Modulation Of Ltp and Maternal Caresupporting

confidence: 57%

Maternal Care and Hippocampal Plasticity: Evidence for Experience-Dependent Structural Plasticity, Altered Synaptic Functioning, and Differential Responsiveness to Glucocorticoids and Stress

Champagne¹,

Bagot²,

Hasselt³

et al. 2008

Journal of Neuroscience

599

478

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Maternal licking and grooming (LG) in infancy influences stress responsiveness and cognitive performance in the offspring. We examined the effects of variation in the frequency of pup LG on morphological, electrophysiological, and behavioral aspects of hippocampal synaptic plasticity under basal and stress-like conditions. We found shorter dendritic branch length and lower spine density in CA1 cells from the adult offspring of low compared with high LG offspring. We also observed dramatic effects on long-term potentiation (LTP) depending on corticosterone treatment. Low LG offspring, in contrast to those of high LG mothers, displayed significantly impaired LTP under basal conditions but surprisingly a significantly enhanced LTP in response to high corticosterone in vitro. This enhanced plasticity under conditions that mimic those of a stressful event was apparent in vivo. Adult low LG offspring displayed enhanced memory relative to high LG offspring when tested in a hippocampal-dependent, contextual fear-conditioning paradigm. Hippocampal levels of glucocorticoid and mineralocorticoid receptors were reduced in low compared with high LG offspring. Such effects, as well as the differences in dendritic morphology, likely contribute to LTP differences under resting conditions, as well as to the maternal effects on synaptic plasticity and behavior in response to elevated corticosterone levels. These results suggest that maternal effects may modulate optimal cognitive functioning in environments varying in demand in later life, with offspring of high and low LG mothers showing enhanced learning under contexts of low and high stress, respectively.

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“…While naïve rats show an enhanced response to corticosterone, handled rats become unresponsive, whereas chronically stressed rats even show a reduced Ca-current amplitude. A comparable importance of the animals' background for the direction of corticosteroid effects was earlier observed in apolipoprotein-E knockout vs wildtype mice (Grootendorst et al, 2001). Similarly, preliminary data show that corticosterone decreases longterm potentiation in rats which received a high degree of maternal care while it enhances long-term potentiation in the offspring of low-care mothers (Champagne et al, 2006).…”

Section: Effect Of Chronic Stress On Ca-currentssupporting

confidence: 54%

Brief RU 38486 Treatment Normalizes the Effects of Chronic Stress on Calcium Currents in Rat Hippocampal CA1 Neurons

Karst

Joëls

2007

Neuropsychopharmacol

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Chronic stress alters many properties in rat brain, like serotonin responsiveness and dendritic morphology. In the present study, we examined (i) whether unpredictable stress during 21 days affects calcium (Ca) currents of CA1 pyramidal neurons recorded on day 22; and (ii) if so, whether this change is normalized by treatment with the glucocorticoid receptor-antagonist RU 38486 during days 18-21. At 3 weeks of unpredictable stress increased the amplitude of the peak and sustained calcium current components, determined in hippocampal slices prepared from animals under rest (ie, with low corticosterone levels). The increased Ca-current amplitude was associated with an enhanced cell capacitance; current density was not significantly affected by chronic stress. In slices from stressed rats that received RU 38486, no stress-induced enhancement of calcium current amplitude was seen, while RU 38486 by itself did not alter calcium currents in handled controls. We confirmed earlier observations that brief in vitro treatment with 100 nM corticosterone, thus substantially activating the low-affinity glucocorticoid receptors, increases Ca-current amplitude recorded 1-4 h later in slices from naïve rats. However, Ca-current amplitude was not affected by corticosterone applied to slices from handled controls and currents were even decreased by corticosterone given to slices from chronically stressed rats, suggesting that corticosterone effects depend on the history of the animal. In conclusion, the data indicate that chronic stress, RU 38486 treatment as well as acute rises in corticosterone level strongly modulate calcium influx into CA1 neurons. This could have consequences for the viability of these neurons.

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Reversal of cognitive deficit of apolipoprotein E knockout mice after repeated exposure to a common environmental experience

Cited by 58 publications

References 50 publications

Lifelong vitamin E intake retards age-associated decline of spatial learning ability in apoE-deficient mice

Lifelong vitamin E intake retards age-associated decline of spatial learning ability in apoE-deficient mice

Maternal Care and Hippocampal Plasticity: Evidence for Experience-Dependent Structural Plasticity, Altered Synaptic Functioning, and Differential Responsiveness to Glucocorticoids and Stress

Brief RU 38486 Treatment Normalizes the Effects of Chronic Stress on Calcium Currents in Rat Hippocampal CA1 Neurons

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