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000257594 041__ $$aEnglish
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000257594 1001_ $$0P:(DE-2719)2810730$$aVarbanov, Hristo$$b0$$eFirst author$$udzne
000257594 245__ $$aRescue of synaptic and cognitive functions in polysialic acid-deficient mice and dementia models by short polysialic acid fragments.
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000257594 520__ $$aDysregulated cortical expression of the neural cell adhesion molecule (NCAM) and deficits of its associated polysialic acid (polySia) have been found in Alzheimer's disease and schizophrenia. However, the functional role of polySia in cortical synaptic plasticity remains poorly understood. Here, we show that acute enzymatic removal of polySia in medial prefrontal cortex (mPFC) slices leads to increased transmission mediated by the GluN1/GluN2B subtype of N-methyl-d-aspartate receptors (NMDARs), increased NMDAR-mediated extrasynaptic tonic currents, and impaired long-term potentiation (LTP). The latter could be fully rescued by pharmacological suppression of GluN1/GluN2B receptors, or by application of short soluble polySia fragments that inhibited opening of GluN1/GluN2B channels. These treatments and augmentation of synaptic NMDARs with the glycine transporter type 1 (GlyT1) inhibitor sarcosine also restored LTP in mice deficient in polysialyltransferase ST8SIA4. Furthermore, the impaired performance of polySia-deficient mice and two models of Alzheimer's disease in the mPFC-dependent cognitive tasks could be rescued by intranasal administration of polySia fragments. Our data demonstrate the essential role of polySia-NCAM in the balancing of signaling through synaptic/extrasynaptic NMDARs in mPFC and highlight the therapeutic potential of short polySia fragments to restrain GluN1/GluN2B-mediated signaling.
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000257594 650_7 $$2Other$$aNCAM
000257594 650_7 $$2Other$$aNMDA receptor
000257594 650_7 $$2Other$$aPolysialic acid
000257594 650_7 $$2Other$$aPrefrontal cortex
000257594 650_7 $$2Other$$aSynaptic plasticity
000257594 650_7 $$2NLM Chemicals$$apolysialic acid
000257594 650_7 $$2NLM Chemicals$$aSialic Acids
000257594 650_7 $$2NLM Chemicals$$aNeural Cell Adhesion Molecules
000257594 650_7 $$2NLM Chemicals$$aReceptors, N-Methyl-D-Aspartate
000257594 650_2 $$2MeSH$$aMice
000257594 650_2 $$2MeSH$$aAnimals
000257594 650_2 $$2MeSH$$aAlzheimer Disease: drug therapy
000257594 650_2 $$2MeSH$$aSialic Acids: metabolism
000257594 650_2 $$2MeSH$$aCognition
000257594 650_2 $$2MeSH$$aNeural Cell Adhesion Molecules: metabolism
000257594 650_2 $$2MeSH$$aReceptors, N-Methyl-D-Aspartate
000257594 7001_ $$0P:(DE-2719)2811420$$aJia, Shaobo$$b1$$udzne
000257594 7001_ $$aKochlamazashvili, Gaga$$b2
000257594 7001_ $$aBhattacharya, Subhrajit$$b3
000257594 7001_ $$aBuabeid, Manal Ali$$b4
000257594 7001_ $$0P:(DE-2719)2811506$$aEl Tabbal, Mohamed$$b5$$udzne
000257594 7001_ $$0P:(DE-2719)2811139$$aHayani, Hussam$$b6$$udzne
000257594 7001_ $$0P:(DE-2719)2809920$$aStoyanov, Stoyan$$b7$$udzne
000257594 7001_ $$0P:(DE-2719)2811509$$aSun, Weilun$$b8$$udzne
000257594 7001_ $$aThiesler, Hauke$$b9
000257594 7001_ $$aRöckle, Iris$$b10
000257594 7001_ $$aHildebrandt, Herbert$$b11
000257594 7001_ $$0P:(DE-2719)2810530$$aSenkov, Oleg$$b12$$udzne
000257594 7001_ $$aSuppiramaniam, Vishnu$$b13
000257594 7001_ $$aGerardy-Schahn, Rita$$b14
000257594 7001_ $$0P:(DE-2719)2810577$$aDityatev, Alexander$$b15$$eLast author$$udzne
000257594 773__ $$0PERI:(DE-600)1471408-5$$a10.1016/j.nbd.2023.106079$$gVol. 180, p. 106079 -$$p106079$$tNeurobiology of disease$$v180$$x0969-9961$$y2023
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