Detection of behavioral alterations and learning deficits in mice lacking synaptophysin

Schmitt, Ulrich; Tanimoto, Naoyuki; Seeliger, M. W.; Schaeffel, Frank; Leube, Rudolf E.

doi:10.1016/j.neuroscience.2009.04.046

Cited by 208 publications

(118 citation statements)

References 43 publications

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“…Mutations in syntaxin-binding protein 1 (STXBP1; Munc-18) have been associated with epileptic encephalopathy, intellectual disability, and movement disorders (45)(46)(47), and recently mutations in syntaxin-1B (STX1B) have also been associated with temperature-sensitive seizure disorders (48), indicating that SNARE complex assembly, SV docking, and priming are important steps in the pathway leading to SV fusion (49). Mice lacking the SV protein synaptophysin (SYP) display behavioral deficits consistent with the association between human SYP mutations and intellectual disability (50,51). Cultured neurons derived from SYP-deficient mice display reduced endocytic rate and SV cargo-retrieval defects (24,52).…”

Section: 7mentioning

confidence: 83%

Identification of a human synaptotagmin-1 mutation that perturbs synaptic vesicle cycling

Baker¹,

Gordon²,

Grozeva³

et al. 2015

J. Clin. Invest.

106

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Section: 7mentioning

confidence: 83%

Identification of a human synaptotagmin-1 mutation that perturbs synaptic vesicle cycling

Baker¹,

Gordon²,

Grozeva³

et al. 2015

J. Clin. Invest.

106

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“…SYN is the major pre-synaptic vesicle protein marker which regulates synaptic function, vesicle fusion, and neurotransmitter release [52]. It has been demonstrated that impairments in learning and memory, most notably reduced object novelty recognition and reduced spatial learning are observed in synaptophysin knockout mice [53]. PSD-95, a major post-synaptic component of synaptic plasticity, is an important regulator of synaptic strength and plasticity [54].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of the orientin on noise-induced cognitive impairments in mice

Wang

Feng

et al. 2016

Behavioural Brain Research

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There is increasing evidence that chronic noise stress impairs cognition and induces oxidative stress in the brain. Recently, orientin, a phenolic compound abundant in some fruits, millet, and herbs, has been shown to have antioxidant properties. This study investigated the potential effects of orientin against chronic noiseinduced cognitive decline and its underlying mechanisms. A moderate-intensity noise exposure model was used to investigate the effects of orientin on behavior and biochemical alterations in mice. After 3 weeks of the noise exposure, the mice were treated with orientin (20 mg/kg and 40 mg/kg, oral gavage) for 3 weeks. The chronic noise exposure impaired the learning and memory in mice in the Morris water maze and step-through tests. The noise exposure also decreased exploration and interest in a novel environment in the open field test. The administration of orientin significantly reversed noise-induced alterations in these behavior tests. Moreover, the orientin treatment significantly improved the noise-induced alteration of serum corticosterone and catecholamine levels and oxidative stress in the hippocampus and prefrontal cortex. Furthermore, the orientin treatment ameliorated the noise-induced decrease in brain-derived neurotrophic factor and synapseassociated proteins (synaptophysin and postsynaptic density protein 95) in the hippocampus and prefrontal cortex. Thus, orientin exerts protective effects on noise-induced cognitive decline in mice, specifically by improving central oxidative stress, neurotransmission, and increases synapse-associated proteins. Therefore, supplementation with orientin-enriched food or fruit could be beneficial as a preventive strategy for chronic noise-induced cognitive decline. Disciplines Medicine and Health Sciences Publication DetailsWang, S., Yu, Y., Feng, Y., Zou, F., Zhang, X., Huang, J., Zhang, Y., Zheng, X., Huang, X., Zhu, Y. & Liu, Y. (2016). Protective effect of the orientin on noise-induced cognitive impairments in mice. Behavioural Brain Research, 296 290-300.

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“…On speculative grounds, however, this difference may be explained by the distinct role of these two presynaptic proteins in 27 governing synaptic strength and neurotransmitter release. The vesicle--associated protein synaptophysin is involved in the regulation of synaptic strength (Han and Stevens, 2009;Schmitt et al, 2009), but it does not seem to be required for the actual release of neurotransmitters from presynaptic vesicles (McMahon et al, 1996). On the other hand, bassoon is a scaffold protein of the presynaptic active zone and critically determines presynaptic neurotransmitter release through various (but not mutually exclusive)…”

mentioning

confidence: 99%

Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies

Giovanoli

Weber‐Stadlbauer

Schedlowski

et al. 2016

Brain, Behavior, and Immunity

122

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Prenatal exposure to infectious or inflammatory insults can increase the risk of developing neuropsychiatric disorder in later life, including schizophrenia, bipolar disorder, and autism. These brain disorders are also characterized by pre-and postsynaptic deficits. Using a well-established mouse model of maternal exposure to the viral mimetic polyriboinosinic-polyribocytidilic acid [poly(I:C)], we examined whether prenatal immune activation might cause synaptic deficits in the hippocampal formation of pubescent and adult offspring. Based on the widely appreciated role of microglia in synaptic pruning, we further explored possible associations between synaptic deficits and microglia anomalies in offspring of poly(I:C)-exposed and control mothers. We found that prenatal immune activation induced an adult onset of presynaptic hippocampal deficits (as evaluated by synaptophysin and bassoon density). The early-life insult further caused postsynaptic hippocampal deficits in pubescence (as evaluated by PSD95 and SynGAP density), some of which persisted into adulthood. In contrast, prenatal immune activation did not change microglia (or astrocyte) density, nor did it alter their activation phenotypes. The prenatal manipulation did also not cause signs of persistent systemic inflammation. Despite the absence of overt glial anomalies or systemic inflammation, adult offspring exposed to prenatal immune activation displayed increased hippocampal IL-1 levels. Taken together, our findings demonstrate that age-dependent synaptic deficits and abnormal pro-inflammatory cytokine expression can occur during postnatal brain maturation in the absence of microglial anomalies or systemic inflammation. AbstractPrenatal exposure to infectious or inflammatory insults can increase the risk of developing neuropsychiatric disorder in later life, including schizophrenia, bipolar disorder, and autism. These brain disorders are also characterized by pre--and postsynaptic deficits.Using a well--established mouse model of maternal exposure to the viral mimetic polyriboinosinic--polyribocytidilic acid [poly(I:C)], we examined whether prenatal immune activation might cause synaptic deficits in the hippocampal formation of pubescent and adult offspring. Based on the widely appreciated role of microglia in synaptic pruning, we further explored possible associations between synaptic deficits and microglia anomalies in offspring of poly(I:C)--exposed and control mothers. We found that prenatal immune activation induced adult onset of presynaptic hippocampal deficits (as evaluated by synaptophysin and bassoon density). The early--life insult further caused postsynaptic hippocampal deficits in pubescence (as evaluated by PSD95 and SynGAP density), some of which persisted into adulthood. In contrast, prenatal immune activation did not change microglia (or astrocyte) density, nor did it alter their activation phenotypes. The prenatal manipulation did also not cause signs of persistent systemic inflammation. Despite the absence of overt glial a...

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Detection of behavioral alterations and learning deficits in mice lacking synaptophysin

Cited by 208 publications

References 43 publications

Identification of a human synaptotagmin-1 mutation that perturbs synaptic vesicle cycling

Identification of a human synaptotagmin-1 mutation that perturbs synaptic vesicle cycling

Protective effect of the orientin on noise-induced cognitive impairments in mice

Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies

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