Decreased hyperlocomotion induced by MK-801, but not amphetamine and caffeine in mice lacking cellular prion protein (PrPC)

Coitinho, Adriana Simon; Dietrich, Marcelo O.; Hoffmann, Ana; Dall'Igna, Oscar Phelippe Permigotti; Souza, Diogo O.; Martins, Vilma R.; Brentani, Ricardo R.; Izquierdo, Iván; Lara, Diogo R.

doi:10.1016/s0169-328x(02)00526-0

Cited by 18 publications

(13 citation statements)

References 36 publications

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“…For example, reduced excitatory post-synaptic potentials (Carleton et al 2001), impaired formation of long-term potentiation (Collinge et al 1994; Criado et al 2005; Manson et al 1995), reductions in after-hyperpolarization potentials (Mallucci et al 2002, Ratte et al 2002) and abnormal responses to NMDA antagonist MK-801 (Coitinho et al 2002) observed in PrPKO mice all suggest attenuation of L-glutamate-mediated signaling. Many of these alterations would be consistent with the premature termination of the L-glutamate signal and/or the excessive clearance of L-glutamate from the extracellular space surrounding EAA receptors.…”

Section: Discussionmentioning

confidence: 99%

Increased excitatory amino acid transport into murine prion protein knockout astrocytes cultured in vitro

Pathmajeyan¹,

Patel

Carroll³

et al. 2011

Glia

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Prion protein (PrP) is expressed on a wide variety of cells and plays an important role in the pathogenesis of transmissible spongiform encephalopathies. However, its normal function remains unclear. Mice that do not express PrP exhibit deficits in spatial memory and abnormalities in excitatory neurotransmission suggestive that PrP may function in the glutamatergic synapse. Here we show that transport of D-aspartate, a non-metabolized L-glutamate analog, through excitatory amino acid transporters (EAATs) was faster in astrocytes from PrP knockout (PrPKO) mice than in astrocytes from C57BL/10SnJ wildtype (WT) mice. Experiments using EAAT subtype-specific inhibitors demonstrated that in both WT and PrPKO astrocytes, the majority of transport was mediated by EAAT1. Furthermore, PrPKO astrocytes were more effective than WT astrocytes at alleviating L-glutamate-mediated excitotoxic damage in both WT and PrPKO neuronal cultures. Thus, in this in vitro model, PrPKO astrocytes exerted a functional influence on neuronal survival and may therefore influence regulation of glutamatergic neurotransmission in vivo.

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Section: Discussionmentioning

confidence: 99%

Increased excitatory amino acid transport into murine prion protein knockout astrocytes cultured in vitro

Pathmajeyan¹,

Patel

Carroll³

et al. 2011

Glia

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“…The day of the test, mice were injected intraperitoneally with ketamine (30 mg/kg; Sigma-Aldrich), amphetamine (1 mg/kg; Sigma-Aldrich), or saline solution, as control. Drug doses were chosen according to previous reports (for ketamine, Irifune et al, 1991Irifune et al, , 1998Behrens et al, 2007;and for amphetamine, Sansone, 1980;Spielewoy et al, 2001;Coitinho et al, 2002). Behavioral test was performed 30 min and 4 h after injection.…”

Section: Methodsmentioning

confidence: 99%

The NADPH Oxidase NOX2 Controls Glutamate Release: A Novel Mechanism Involved in Psychosis-Like Ketamine Responses

Sorce¹,

Schiavone²,

Tucci³

et al. 2010

J. Neurosci.

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Subanesthetic doses of NMDA receptor antagonist ketamine induce schizophrenia-like symptoms in humans and behavioral changes in rodents. Subchronic administration of ketamine leads to loss of parvalbumin-positive interneurons through reactive oxygen species (ROS), generated by the NADPH oxidase NOX2. However, ketamine induces very rapid alterations, in both mice and humans. Thus, we have investigated the role of NOX2 in acute responses to subanesthetic doses of ketamine. In wild-type mice, ketamine caused rapid (30 min) behavioral alterations, release of neurotransmitters, and brain oxidative stress, whereas NOX2-deficient mice did not display such alterations. Decreased expression of the subunit 2A of the NMDA receptor after repetitive ketamine exposure was also precluded by NOX2 deficiency. However, neurotransmitter release and behavioral changes in response to amphetamine were not altered in NOX2-deficient mice. Our results suggest that NOX2 is a major source of ROS production in the prefrontal cortex controlling glutamate release and associated behavioral alterations after acute ketamine exposure. Prolonged NOX2-dependent glutamate release may lead to neuroadaptative downregulation of NMDA receptor subunits.

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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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Decreased hyperlocomotion induced by MK-801, but not amphetamine and caffeine in mice lacking cellular prion protein (PrPC)

Cited by 18 publications

References 36 publications

Increased excitatory amino acid transport into murine prion protein knockout astrocytes cultured in vitro

Increased excitatory amino acid transport into murine prion protein knockout astrocytes cultured in vitro

The NADPH Oxidase NOX2 Controls Glutamate Release: A Novel Mechanism Involved in Psychosis-Like Ketamine Responses

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

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