Hippocampal Dysfunction in Schizophrenia and Aberrant Hippocampal
                    Synaptic Plasticity in Rodent Model Psychosis: a Selective
                    Review

Bartsch, Julia; Schott, Björn H.; Behr, Jüergen

doi:10.1055/a-0960-9846

Cited by 6 publications

(5 citation statements)

References 92 publications

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“…Bearing in mind the pivotal role of the subiculum as information gatekeeper between the hippocampus and other brain regions, this aberrant LTP in ventral subicular regularfiring neurons is expected to interfere with physiological hippocampal output processing. Thereby, our results add to the notion from previous rodent studies suggesting that subregion-specific reduced synaptic plasticity or aberrant hyperplasticity contributes to hippocampal dysfunction in firstepisode psychosis (Tamminga et al, 2012a;Bartsch et al, 2019). Moreover, our observation of a cell type-specific facilitation of subicular LTP after systemic NMDAR antagonism can be considered as a form of metaplasticity.…”

Section: Possible Functional Impact Of the Aberrant Noncanonical Ltp supporting

confidence: 86%

Noncanonical, Dopamine-Dependent Long-Term Potentiation at Hippocampal Output Synapses in a Rodent Model of First-Episode Psychosis

Bartsch

Behr

2020

Front. Mol. Neurosci.

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Cognitive deficits and positive symptoms in schizophrenia have both been linked to hippocampal dysfunction. Recently, subregion-specific aberrant and maladaptive hippocampal synaptic plasticity has been suggested as one of the mechanistic underpinnings. The subiculum is the final output hub of the hippocampus and orchestrates hippocampal information transfer to other brain regions. While most CA1 pyramidal neurons show regular-spiking behavior, subicular output neurons comprise bursting and regular-firing pyramidal cells. These two cell types target different brain regions and express unique forms of synaptic plasticity. Here, we used a single systemic application of the noncompetitive glutamatergic N-methyl-D-aspartate receptor (NMDAR) antagonist MK-801 to model first-episode psychosis in rats and studied long-term potentiation (LTP) in subicular regular-firing cells in acute hippocampal slices. Previously, we have reported a facilitation of a presynaptic, late-onset LTP in subicular bursting pyramidal cells after systemic NMDAR antagonism. Here, we show that single systemic NMDAR antagonist application also facilitates the induction of a noncanonical, but postsynaptic NMDAR-independent LTP in ventral subicular but not in CA1 regular-firing pyramidal cells. This form of LTP was dependent on D1/D5 dopamine receptor activation. Activation of D1/D5 dopamine receptors by a specific agonist mimicked and occluded LTP induced by electrical high-frequency stimulation (HFS). Furthermore, our results indicate that this form of LTP relies on postsynaptic Ca 2+ signaling and requires the activation of protein kinase A. Considering the pivotal role of the subiculum as information gatekeeper between the hippocampus and other brain regions, this aberrant LTP in ventral subicular regular-firing neurons is expected to interfere with physiological hippocampal output processing and might thereby contribute to hippocampal dysfunction in psychotic events.

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Section: Possible Functional Impact Of the Aberrant Noncanonical Ltp supporting

confidence: 86%

Noncanonical, Dopamine-Dependent Long-Term Potentiation at Hippocampal Output Synapses in a Rodent Model of First-Episode Psychosis

Bartsch

Behr

2020

Front. Mol. Neurosci.

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“…Accumulated studies have demonstrated that hippocampal and cortical LTP was impaired in both patients and animal models of schizophrenia, a fact that is thought to be closely correlated with the cognitive impairments (Bartsch et al, 2019;Stephan et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…LTP is one of the core manifestations of synaptic plasticity and widely considered as a cellular basis of learning and memory (Lynch, 2004). Accumulated studies have demonstrated that hippocampal and cortical LTP was impaired in both patients and animal models of schizophrenia, a fact that is thought to be closely correlated with the cognitive impairments (Bartsch et al., 2019; Stephan et al., 2006).…”

Section: Introductionmentioning

confidence: 99%

Flavonoid fisetin reverses impaired hippocampal synaptic plasticity and cognitive function by regulating the function of AMPARs in a male rat model of schizophrenia

Zhan

Chen

et al. 2021

Journal of Neurochemistry

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Cognitive deficits are the core feature of schizophrenia and effective treatment strategies are still missing. Previous studies have reported that fisetin promotes long-term potentiation (LTP) and cognitive function in normal rodents and other model animals of neurological diseases. The aim of this study was to assess the effect of fisetin on How to cite this article: Zhan J-Q, Chen C-N, Wu S-X, et al.Flavonoid fisetin reverses impaired hippocampal synaptic plasticity and cognitive function by regulating the function of AMPARs in a male rat model of schizophrenia.

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“…More broadly, our results suggest that reduced Ncan expression might contribute to an altered excitation-inhibition ratio hypothesized to be a key circuit mechanism in the major psychoses (Howes & Shatalina, 2022; Grent-’t-Jong et al, 2023), which, at a systems level, may be reflected by a manic phenotype (Miro et al, 2012) and tonically increased hippocampal activity (Bartsch et al, 2023; Assmann et al, 2021).…”

Section: Discussionmentioning

confidence: 76%

Neurocan regulates axon initial segment organization and neuronal activity in cultured cortical neurons

Baidoe-Ansah,

Mirzapourdelavar,

Aleshin

et al. 2024

Preprint

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The neural extracellular matrix (ECM) accumulates in the form of perineuronal nets (PNNs), particularly around fast-spiking GABAergic interneurons in the cortex and hippocampus, but also in association with the axon initial segments (AIS) and nodes of Ranvier. Increasing evidence highlights the role of Neurocan (Ncan), a brain-specific component of ECM, in the pathophysiology of neuropsychiatric disorders like bipolar disorder and schizophrenia. Ncan localizes at PNNs, nodes of Ranvier and the AIS, highlighting its potential role in regulation of axonal excitability. Here, we used knockdown and knockout approaches in mouse primary cortical neurons in combination with immunocytochemistry, western blotting and electrophysiological techniques to characterize the role of Ncan in the organization of PNNs and AIS and in the regulation of neuronal activity. We found that reduced Ncan levels led to remodeling of PNNs around neurons via upregulated Aggrecan mRNA and protein levels, increased expression of activity-dependent c-Fos and FosB genes and elevated spontaneous synaptic activity. The latter correlated with increased levels of Ankyrin-G in the AIS particularly in excitatory neurons, and with the elevated expression of Nav1.6 channels. Our results suggest that Ncan regulate expression of key proteins in PNNs and AISs and provide new insights into its role in the fine-tuning of neuronal functions.

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Hippocampal Dysfunction in Schizophrenia and Aberrant Hippocampal Synaptic Plasticity in Rodent Model Psychosis: a Selective Review

Cited by 6 publications

References 92 publications

Noncanonical, Dopamine-Dependent Long-Term Potentiation at Hippocampal Output Synapses in a Rodent Model of First-Episode Psychosis

Noncanonical, Dopamine-Dependent Long-Term Potentiation at Hippocampal Output Synapses in a Rodent Model of First-Episode Psychosis

Flavonoid fisetin reverses impaired hippocampal synaptic plasticity and cognitive function by regulating the function of AMPARs in a male rat model of schizophrenia

Neurocan regulates axon initial segment organization and neuronal activity in cultured cortical neurons

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