Ammonia-mediated LTP inhibition: Effects of NMDA receptor antagonists and l-carnitine

Izumi, Yukitoshi; Izumi, Masayo; Matsukawa, Mio; Funatsu, M.; Zorumski, Charles F.

doi:10.1016/j.nbd.2005.04.013

Cited by 24 publications

(20 citation statements)

References 49 publications

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“…Multiple metabolic insults can produce acute memory impairment and altered cognition, including hypoxia/ischemia, hypoglycemia, and renal and hepatic insufficiency among others. The findings that NMDAR-mediated LTP inhibition is associated with brief hypoxia (Izumi et al, 1998), low glucose (Izumi and Zorumski, 1997) and elevated ammonia (Izumi et al, 2005a) are consistent with a role in cognitive dysfunction associated with these conditions, and raise the possibility that this may be a general mechanism contributing to similar clinical states. In the context of organ failure, metabolic stress, sometimes involving the accumulation of endogenous or exogenous toxins (such as ammonia in the case of liver failure) manifests, at least in part, via increases in extracellular glutamate and possibly the metaplastic changes outlined here (Beal et al, 1993; Lipton, 1999; Marcaida et al, 1992; Nishizawa, 2001).…”

Section: Does Nmdar-mediated Ltp Inhibition Extend To Other Conditmentioning

confidence: 82%

“…Other studies demonstrated links between LTP inhibition and conditions of neuronal stress. In particular, brief bouts of hypoxia in the presence of normal glucose (Izumi et al, 1998), low glucose alone (mimicking mild hypoglycemia) (Izumi and Zorumski, 1997) or exposure to ammonia (mimicking hepatotoxic states) (Izumi et al, 2005a) all resulted in impaired LTP induction in which basal neurotransmission was not persistently altered and in which NMDAR antagonists administered during the insult overcame the LTP inhibition. Later studies showed that treatments that relieved negative regulation of NMDARs by extracellular zinc (e.g.…”

Section: Nmdar-mediated Ltp Inhibition: a Specific Form Of Metaplamentioning

confidence: 99%

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NMDA receptors and metaplasticity: Mechanisms and possible roles in neuropsychiatric disorders

Zorumski

Izumi

2012

Neuroscience & Biobehavioral Reviews

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105

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N-methyl-D-aspartate receptors (NMDARs) are key components of neural signaling, playing roles in synaptic transmission and in the synaptic plasticity thought to underlie learning and memory. NMDAR activation can also have neurotoxic consequences contributing to several forms of neurodegeneration. Additionally, NMDARs can modulate neuronal function and regulate the ability of synapses to undergo synaptic plasticity. Evidence gathered over the past 20 years strongly supports the idea that untimely activation of NMDARs impairs the induction of long-term potentiation (LTP) by a form of metaplasticity. This metaplasticity can be triggered by multiple stimuli including physiological receptor activation, and metabolic and behavioral stressors. These latter findings raise the possibility that NMDARs contribute to cognitive dysfunction associated with neuropsychiatric disorders. This paper examines NMDAR metaplasticity and its potential role in cognition. Recent studies using NMDAR antagonists for therapeutic purposes also raise the possibility that metaplasticity may contribute to clinical effects of certain drugs.

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Section: Does Nmdar-mediated Ltp Inhibition Extend To Other Conditmentioning

confidence: 82%

Section: Nmdar-mediated Ltp Inhibition: a Specific Form Of Metaplamentioning

confidence: 99%

NMDA receptors and metaplasticity: Mechanisms and possible roles in neuropsychiatric disorders

Zorumski

Izumi

2012

Neuroscience & Biobehavioral Reviews

Self Cite

113

105

View full text Add to dashboard Cite

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“…This effect is observed with low concentrations of NMDA (e.g., 1 μM × 5 min) that produce no change in basal AMPAR-mediated synaptic transmission (Izumi, Clifford, & Zorumski, 1992a). Persistent LTP block is also achieved by mildly stressful metabolic conditions including low glucose (Izumi & Zorumski, 1997), brief hypoxia (Izumi, Katsuki, Benz, & Zorumski, 1998), and ammonia (Izumi, Izumi, Matsukawa, Funatsu, & Zorumski, 2005a), and following behavioral stress (Kim, Foy, & Thompson, 1996; Yang, Yang, Huang, & Hsu, 2008). In all of these examples, an NMDAR antagonist administered during the stressor paradoxically promotes LTP, implicating untimely, low-level NMDAR activation in LTP inhibition.…”

Section: Do Metaplastic Effects Contribute To Acute Ltp Inhibition?mentioning

confidence: 99%

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Zorumski¹,

Mennerick²,

Izumi³

2014

Alcohol

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113

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Alcoholism is associated with acute and long-term cognitive dysfunction including memory impairment, resulting in substantial disability and cost to society. Thus, understanding how ethanol impairs cognition is essential for developing treatment strategies to dampen its adverse impact. Memory processing is thought to involve persistent, use-dependent changes in synaptic transmission, and ethanol alters the activity of multiple signaling molecules involved in synaptic processing, including modulation of the glutamate and gamma-aminobutyric acid (GABA) transmitter systems that mediate most fast excitatory and inhibitory transmission in the brain. Effects on glutamate and GABA receptors contribute to ethanol-induced changes in long-term potentiation (LTP) and long-term depression (LTD), forms of synaptic plasticity thought to underlie memory acquisition. In this paper, we review the effects of ethanol on learning-related forms of synaptic plasticity with emphasis on changes observed in the hippocampus, a brain region that is critical for encoding contextual and episodic memories. We also include studies in other brain regions as they pertain to altered cognitive and mental function. Comparison of effects in the hippocampus to other brain regions is instructive for understanding the complexities of ethanol’s acute and long-term pharmacological consequences.

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“…Studies of NMDAR-dependent LTP in the hippocampus showed that the major features of LTP deficits observed in animal models of chronic hyperammonemia and HE [35,36] can be reproduced by long in vitro exposure of hippocampal slices to ammonium ions [34,[36][37][38]. In our previous study on mouse brain slice preparations we used a similar in vitro model to analyze the effects of hyperammonemia on the characteristics of corticostriatal longterm depression (LTD) induced by electrical stimulation of cortical input or pharmacological activation of mGluR I.…”

Section: Introductionmentioning

confidence: 99%

Alterations of corticostriatal plasticity by ammonium and rescue by green tea polyphenols

Chepkova¹,

Sergeeva²,

Haas³

2013

Archives of Biochemistry and Biophysics

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Ammonia-mediated LTP inhibition: Effects of NMDA receptor antagonists and l-carnitine

Cited by 24 publications

References 49 publications

NMDA receptors and metaplasticity: Mechanisms and possible roles in neuropsychiatric disorders

NMDA receptors and metaplasticity: Mechanisms and possible roles in neuropsychiatric disorders

Acute and chronic effects of ethanol on learning-related synaptic plasticity

Alterations of corticostriatal plasticity by ammonium and rescue by green tea polyphenols

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