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

Chepkova, A. N.; Sergeeva, Olga A.; Haas, Helmut L.

doi:10.1016/j.abb.2013.02.002

Cited by 6 publications

(3 citation statements)

References 80 publications

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“…Whereas hippocampal LTD induced pharmacologically by application of either NMDA or the group I mGluR agonist DHPG was not changed at all, a reversal of NMDA-induced LTD and a significant decrease in the magnitude of LTD induced by DHPG was found in the striatum of LGS-ko mice. Similar modifications of chemically-induced LTD were previously observed in an in vitro model of hyperammonemia with long preincubation of corticostriatal slices with ammonium chloride6566. Resistance of hippocampal NMDA-LTD to high ammonia conditions is in line with previous data in another in vitro model of hyperammonemia43: a brief pulse of NMDA had readily induced chemical LTD in dissociated hippocampal cultures at DIV14–16 independent of prior ammonium chloride or sham treatment for 36 h.…”

Section: Discussionsupporting

confidence: 87%

Impaired novelty acquisition and synaptic plasticity in congenital hyperammonemia caused by hepatic glutamine synthetase deficiency

Chepkova

Sergeeva

Görg

et al. 2017

Sci Rep

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Genetic defects in ammonia metabolism can produce irreversible damage of the developing CNS causing an impairment of cognitive and motor functions. We investigated alterations in behavior, synaptic plasticity and gene expression in the hippocampus and dorsal striatum of transgenic mice with systemic hyperammonemia resulting from conditional knockout of hepatic glutamine synthetase (LGS-ko). These mice showed reduced exploratory activity and delayed habituation to a novel environment. Field potential recordings from LGS-ko brain slices revealed significantly reduced magnitude of electrically-induced long-term potentiation (LTP) in both CA3-CA1 hippocampal and corticostriatal synaptic transmission. Corticostriatal but not hippocampal slices from LGS-ko brains demonstrated also significant alterations in long-lasting effects evoked by pharmacological activation of glutamate receptors. Real-time RT-PCR revealed distinct patterns of dysregulated gene expression in the hippocampus and striatum of LGS-ko mice: LGS-ko hippocampus showed significantly modified expression of mRNAs for mGluR1, GluN2B subunit of NMDAR, and A1 adenosine receptors while altered expression of mRNAs for D1 dopamine receptors, the M1 cholinoreceptor and the acetylcholine-synthetizing enzyme choline-acetyltransferase was observed in LGS-ko striatum. Thus, inborn systemic hyperammonemia resulted in significant deficits in novelty acquisition and disturbed synaptic plasticity in corticostriatal and hippocampal pathways involved in learning and goal-directed behavior.

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Section: Discussionsupporting

confidence: 87%

Impaired novelty acquisition and synaptic plasticity in congenital hyperammonemia caused by hepatic glutamine synthetase deficiency

Chepkova

Sergeeva

Görg

et al. 2017

Sci Rep

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“…Sun et al ( 2017 ) showed that high-intensity treadmill running impaired the mice’ spatial memory and hippocampal synaptic plasticity. Corticostriatal synaptic plasticity plays a crucial role in modulating motor activity, and is the cellular basis of motor skill learning and cognitive performance (Calabresi et al, 1996 ; Mahon et al, 2004 ; Chepkova et al, 2013 ). However, to our knowledge, no studies have reported the effect of EF on corticostriatal synaptic plasticity.…”

Section: Introductionmentioning

confidence: 99%

Exercise-Induced Fatigue Impairs Bidirectional Corticostriatal Synaptic Plasticity

Chen

Liu

et al. 2018

Front. Cell. Neurosci.

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Exercise-induced fatigue (EF) is a ubiquitous phenomenon in sports competition and training. It can impair athletes' motor skill execution and cognition. Corticostriatal synaptic plasticity is considered to be the cellular mechanism of movement control and motor learning. However, the effect of EF on corticostriatal synaptic plasticity remains elusive. In the present study, using field excitatory postsynaptic potential recording, we found that the corticostriatal long-term potentiation (LTP) and long-term depression (LTD) were both impaired in EF mice. To further investigate the cellular mechanisms underlying the impaired synaptic plasticity in corticostriatal pathway, whole-cell patch clamp recordings were carried out on striatal medium spiny neurons (MSNs). MSNs in EF mice exhibited increased spontaneous excitatory postsynaptic current (sEPSC) frequency and decreased paired-pulse ratio (PPR), while with normal basic electrophysiological properties and normal sEPSC amplitude. Furthermore, the N-methyl-D-aspartate (NMDA)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) ratio of MSNs was reduced in EF mice. These results suggest that the enhanced presynaptic glutamate (Glu) release and downregulated postsynaptic NMDA receptor function lead to the impaired corticostriatal plasticity in EF mice. Taken together, our findings for the first time show that the bidirectional corticostriatal synaptic plasticity is impaired after EF, and suggest that the aberrant corticostriatal synaptic plasticity may be involved in the production and/or maintenance of EF.

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“…Our earlier studies showed a reduction of long-lasting depression in response to histamine (LLDhist) in rats with portacaval anastomosis, 10 but no change in LLDhist after the treatment of in vitro slices with ammonium chloride (5 mM) for 4-8 hours. 22 The symptoms of hyperammonemia alone do not reflect the symptoms of HE sufficiently well.…”

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confidence: 99%

Histamine‐induced plasticity and gene expression in corticostriatal pathway under hyperammonemia

et al. 2019

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Aims Histamine H3 receptor (H3R) antagonists/inverse agonists increase vigilance. We studied brain histaminergic pathways under hyperammonemia and the transcriptome of receptors and their signaling cascades to provide a rationale for wake‐promoting therapies. Methods We analyzed histamine‐induced long‐lasting depression of corticostriatal synaptic transmission (LLDhist). As the expression of dopamine 1 receptors (D1R) is upregulated in LGS‐KO striatum where D1R‐H3R dimers may exist, we investigated actions of H3R and D1R agonists and antagonists. We analyzed transcription of selected genes in cortex and dorsal striatum in a mouse model of inborn hyperammonemia (liver‐specific glutamine synthetase knockout: LGS‐KO) and compared it with human hepatic encephalopathy. Results LGS‐KO mice showed significant reduction of the direct depression (DD) but not the long‐lasting depression (LLD) by histamine. Neither pharmacological activation nor inhibition of D1R significantly affected DDhist and LLDhist in WT striatum, while in LGS‐KO mice D1R activation suppressed LLDhist. Histaminergic signaling was found unchanged at the transcriptional level except for the H2R. A study of cAMP‐regulated genes indicated a significant reduction in the molecular signature of wakefulness in the diseased cortex. Conclusions Our findings provide a rationale for the development of aminergic wake‐promoting therapeutics in hyperammonemic disorders.

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

Cited by 6 publications

References 80 publications

Impaired novelty acquisition and synaptic plasticity in congenital hyperammonemia caused by hepatic glutamine synthetase deficiency

Impaired novelty acquisition and synaptic plasticity in congenital hyperammonemia caused by hepatic glutamine synthetase deficiency

Exercise-Induced Fatigue Impairs Bidirectional Corticostriatal Synaptic Plasticity

Histamine‐induced plasticity and gene expression in corticostriatal pathway under hyperammonemia

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