Altered behavioural response to acute stress in mice lacking cellular prion protein

Nico, Patrícia Barreto Costa; de‐Paris, Fernanda; Vinadé, Elsa Regina; Amaral, Olavo B.; Rockenbach, Isabel Cristina; Lobão-Soares, Bruno; Guarnieri, Ricardo; Wichert‐Ana, Lauro; Calvo, Fabrício; Walz, Roger; Izquierdo, Iván; Sakamoto, Américo Ceiki; Brentani, Ricardo R.; Martins, Vilma R.; Bianchin, Marino Muxfeldt

doi:10.1016/j.bbr.2005.02.003

Cited by 46 publications

(37 citation statements)

References 59 publications

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“…In the present study, stress acted as an ideal physiological trigger instead of pharmacological triggers to induce plaque disruption. Previous studies have confirmed that both electric foot shock and noise stimulation are effective stressors for mice (8,13,23,24,27,35,44). Besides the hemodynamic effects, foot shock stress also affects inflammatory (8) and immunologic (24) function.…”

Section: Discussionmentioning

confidence: 94%

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

N¹,

Wang²,

Zhang³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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To establish an animal model with disruptions of atherosclerotic plaques, 96 male apolipoprotein E knockout (apoE(-/-)) mice were randomly divided into stress, lipopolysaccharide (LPS), stress+LPS, and control groups (n = 24 each). All mice were fed a high-fat diet throughout the experiment, and carotid atherosclerotic lesions were induced by placement of a constrictive perivascular collar. Four weeks after surgery, mice in the LPS and stress+LPS groups were intraperitoneally injected with LPS (1 mg/kg twice per week for 8 wk). Eight weeks after surgery, mice in the stress and stress+LPS groups were treated with intermittent physical stress (electric foot shock and noise stimulation) for 4 wk. Morphological analysis revealed a plaque disruption rate of 16.7% in control, 34.8% in LPS, 54.2% in stress, and 60.9% in stress+LPS groups. The disruption rates in stress and stress+LPS groups were both significantly higher than those of controls (P = 0.007 and P = 0.002, respectively). Luminal thrombosis secondary to plaque disruption was observed only in the stress+LPS group. Both stress and LPS stimulation significantly decreased fibrous cap thickness and increased macrophage and lipid contents in plaques. Moreover, the combination of stress and LPS stimulation further lowered cap thickness and enhanced accumulation of macrophages and expression of inflammatory cytokines and matrix metalloproteinases. Stress activated the sympathetic nervous system, as manifested by increased blood pressure and flow velocity. Plasma fibrinogen levels were remarkably elevated in the stress and stress+LPS groups. In conclusion, stress- and LPS-costimulated apoE(-/-) mice provide a useful model for studies of plaque vulnerability and interventions.

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Section: Discussionmentioning

confidence: 94%

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

N¹,

Wang²,

Zhang³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…The behavior of PrP-deficient mice supports this prediction. Compared to wild-type controls, Nico et al (30) found that PrP-deficient animals have lower swimming capacities and less locomotor activity after bouts of forced exercise. In a separate study (31), the authors challenged mice with forced swimming under different loads and found that PrP-deficient animals could swim for less time.…”

Section: Introductionmentioning

confidence: 99%

Prion Protein Expression and Functional Importance in Skeletal Muscle

Smith

Moylan

Hardin

et al. 2011

Antioxidants & Redox Signaling

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Skeletal muscle expresses prion protein (PrP) that buffers oxidant activity in neurons. Aims: We hypothesize that PrP deficiency would increase oxidant activity in skeletal muscle and alter redox-sensitive functions, including contraction and glucose uptake. We used real-time polymerase chain reaction and Western blot analysis to measure PrP mRNA and protein in human diaphragm, five murine muscles, and muscle-derived C2C12 cells.Effects of PrP deficiency were tested by comparing PrP-deficient mice versus wild-type mice and morpholinoknockdown versus vehicle-treated myotubes. Oxidant activity (dichlorofluorescin oxidation) and specific force were measured in murine diaphragm fiber bundles. Results: PrP content differs among mouse muscles (gastrocnemius > extensor digitorum longus, EDL > tibialis anterior, TA; soleus > diaphragm) as does glycosylation (di-, mono-, nonglycosylated; gastrocnemius, EDL, TA = 60%, 30%, 10%; soleus, 30%, 40%, 30%; diaphragm, 30%, 30%, 40%). PrP is predominantly di-glycosylated in human diaphragm. PrP deficiency decreases body weight (15%) and EDL mass (9%); increases cytosolic oxidant activity (fiber bundles, 36%; C2C12 myotubes, 7%); and depresses specific force (12%) in adult (8-12 mos) but not adolescent (2 mos) mice. Innovation: This study is the first to directly assess a role of prion protein in skeletal muscle function. Conclusions: PrP content varies among murine skeletal muscles and is essential for maintaining normal redox homeostasis, muscle size, and contractile function in adult animals. Antioxid. Redox Signal. 15, 2465-2475.

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“…Information on the phenotypes of PrP-knockout mice has been accumulated, and include slight abnormalities such as aberrant circadian rhythms [110][111][112][113], altered locomotion [114][115][116], deficits in spatial learning and memory, and high susceptibility to seizure [117] and brain injury [118,119] in Prnp-knockout mice. Electrophysiological abnormality was also reported [120][121][122][123][124][125][126][127][128][129][130][131], but remains controversial [130][131].…”

Section: Study Of Prp By Gene Targeting Methodsmentioning

confidence: 99%

“…Altered calcium homeostasis ZrchI [144,145] Altered circadian rhythms ZrchI [110][111][112][113] Altered cytokine production and proliferation Rikn, Npu [149,150] Altered locomotion ZrchI [114][115][116] Cellular copper content Rikn, ZrchI, Npu [17,129,143] [164]…”

Section: Study Of Prp By Gene Targeting Methodsmentioning

confidence: 99%

Recent Advances in Clarifying Prion Protein Functions Using Knockout Mice and Derived Cell Lines

Sakudo¹,

Onodera²,

Suganuma³

et al. 2006

MRMC

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Considerable information on the functions of prion protein (PrP) has been accumulated. One experimental approach is the use of PrP gene-knockout mice and derived cell lines. This approach has contributed to elucidating the functions of cellular prion protein (PrP(C)), such as its anti-oxidative and anti-apoptotic roles. This review will introduce the recent advances in prion biology made possible by the availability of these tools.

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Altered behavioural response to acute stress in mice lacking cellular prion protein

Cited by 46 publications

References 59 publications

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

Prion Protein Expression and Functional Importance in Skeletal Muscle

Recent Advances in Clarifying Prion Protein Functions Using Knockout Mice and Derived Cell Lines

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