PSD-95 in CA1 Area Regulates Spatial Choice Depending on Age

Cały, Anna; Śliwińska, Małgorzata Alicja; Ziółkowska, Magdalena; Łukasiewicz, Kacper; Pagano, Roberto; Dzik, Jakub M.; Kalita, Katarzyna; Bernaś, Tytus; Stewart, Michael G.; Giese, K. Peter; Radwańska, Kasia

doi:10.1523/jneurosci.1996-20.2020

Cited by 13 publications

(10 citation statements)

References 72 publications

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“…PSD-95 is a major synaptic protein involved in aging ( Savioz et al, 2014 ; Bustos et al, 2017 ). In this study, hippocampal Psd-95 expression decreased with aging, which has been confirmed in other experiments ( Rogers et al, 2017 ; Cały et al, 2021 ).…”

Section: Discussionsupporting

confidence: 91%

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Zhang²,

Li³

et al. 2022

Front. Aging Neurosci.

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IntroductionResearch suggests that prenatal inflammatory exposure could accelerate age-related cognitive decline that may be resulted from neuroinflammation and synaptic dysfunction during aging. Environmental enrichment (EE) may mitigate the cognitive and synaptic deficits. Neurite growth-promoting factor 2 (NGPF2) and postsynaptic density protein 95 (PSD-95) play critical roles in neuroinflammation and synaptic function, respectively.MethodsWe examined whether this adversity and EE exposure can cause alterations in Ngpf2 and Psd-95 expression. In this study, CD-1 mice received intraperitoneal injection of lipopolysaccharide (50 μg/kg) or normal saline from gestational days 15–17. After weaning, half of the male offspring under each treatment were exposed to EE. The Morris water maze was used to assess spatial learning and memory at 3 and 15 months of age, whereas quantitative real-time polymerase chain reaction and Western blotting were used to measure hippocampal mRNA and protein levels of NGPF2 and PSD-95, respectively. Meanwhile, serum levels of IL-6, IL-1β, and TNF-α were determined by enzyme-linked immunosorbent assay.ResultsThe results showed that aged mice exhibited poor spatial learning and memory ability, elevated NGPF2 mRNA and protein levels, and decreased PSD-95 mRNA and protein levels relative to their young counterparts during natural aging. Embryonic inflammatory exposure accelerated age-related changes in spatial cognition, and in Ngpf2 and Psd-95 expression. Additionally, the levels of Ngpf2 and Psd-95 products were significantly positively and negatively correlated with cognitive dysfunction, respectively, particularly in prenatal inflammation-exposed aged mice. Changes in serum levels of IL-6, IL-1β, and TNF-α reflective of systemic inflammation and their correlation with cognitive decline during accelerated aging were similar to those of hippocampal NGPF2. EE exposure could partially restore the accelerated decline in age-related cognitive function and in Psd-95 expression, especially in aged mice.DiscussionOverall, the aggravated cognitive disabilities in aged mice may be related to the alterations in Ngpf2 and Psd-95 expression and in systemic state of inflammation due to prenatal inflammatory exposure, and long-term EE exposure may ameliorate this cognitive impairment by upregulating Psd-95 expression.

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Section: Discussionsupporting

confidence: 91%

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Zhang²,

Li³

et al. 2022

Front. Aging Neurosci.

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“…Mice were 2–6 months old at the beginning of the experiments. Only female mice were used in the experiments in the IntelliCages, as males are too aggressive for group housing 55–57 . In other experiments, mice of both sexes were used (sexes were equally distributed between the experimental groups).…”

Section: Methodsmentioning

confidence: 99%

Autophosphorylation of αCaMKII regulates alcohol consumption by controlling sedative effects of alcohol and alcohol‐induced loss of excitatory synapses

et al. 2023

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Calcium/calmodulin‐dependent kinase II (CaMKII) is a key enzyme at the glutamatergic synapses. CAMK2A gene variants have been linked with alcohol use disorder (AUD) by an unknown mechanism. Here, we looked for the link between αCaMKII autophosphorylation and the AUD aetiology. Autophosphorylation‐deficient heterozygous αCaMKII mutant mice (T286A+/−) were trained in the IntelliCages to test the role of αCaMKII activity in AUD‐related behaviours. The glutamatergic synapses morphology in CeA was studied in the animals drinking alcohol using 3D electron microscopy. We found that T286A+/− mutants consumed less alcohol and were more sensitive to sedating effects of alcohol, as compared to wild‐type littermates (WT). After voluntary alcohol drinking, T286A+/− mice had less excitatory synapses in the CeA, as compared to alcohol‐naive animals. This change correlated with alcohol consumption was not reversed after alcohol withdrawal and not observed in WT mice. Our study suggests that αCaMKII autophosphorylation affects alcohol consumption by controlling sedative effects of alcohol and preventing synaptic loss in the individuals drinking alcohol. This finding advances our understanding of the molecular processes that regulate alcohol dependence.

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“…Mice were 2-6 months old at the beginning of the experiments. Only female mice were used in the experiments in the IntelliCages, as males are too aggressive for group housing [54][55][56]. In other experiments mice of both sexes were used (sexes were equally distributed between the experimental groups).…”

Section: Animalsmentioning

confidence: 99%

Autophosphorylation of αCaMKII regulates alcohol consumption by controlling sedative effects of alcohol and alcohol-induced loss of excitatory synapses

Cały

Ziółkowska

Pagano

et al. 2023

Preprint

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Calcium/calmodulin-dependent kinase II (CaMKII) is a key enzyme at the glutamatergic synapses. CAMK2A gene variants have been linked with alcohol use disorder (AUD) by an unknown mechanism. Here, we looked for the link between αCaMKII autophosphorylation and the AUD etiology. Autophosphorylation-deficient heterozygous αCaMKII mutant mice (T286A+/-) were trained in the IntelliCages to test the role of αCaMKII activity in AUD-related behaviors. The glutamatergic synapses morphology in CeA was studied in the animals drinking alcohol using 3D electron microscopy. We found that T286A+/- mutants consumed less alcohol and were more sensitive to sedating effects of alcohol, as compared to wild-type littermates (WT). After voluntary alcohol drinking T286A+/- mice had less excitatory synapses in the CeA, as compared to alcohol-naive animals. This change correlated with alcohol consumption, was not reversed after alcohol withdrawal and not observed in WT mice. Our study suggests that αCaMKII autophosphorylation affects alcohol consumption by controlling sedative effects of alcohol and preventing synaptic loss in the individuals drinking alcohol. This finding advances our understanding of the molecular processes that regulate alcohol misuse.

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PSD-95 in CA1 Area Regulates Spatial Choice Depending on Age

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Cited by 13 publications

References 72 publications

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95

Autophosphorylation of αCaMKII regulates alcohol consumption by controlling sedative effects of alcohol and alcohol‐induced loss of excitatory synapses

Autophosphorylation of αCaMKII regulates alcohol consumption by controlling sedative effects of alcohol and alcohol-induced loss of excitatory synapses

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