CaMKII Isoforms in Learning and Memory: Localization and Function

Zalcman, Gisela; Federman, Noel; Romano, Arturo

doi:10.3389/fnmol.2018.00445

Cited by 133 publications

(104 citation statements)

References 127 publications

(183 reference statements)

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“…These results suggest that integrin β1 participates in the regulation of spine changes by Aβ oligomers. A key actin-binding protein in the calcium signaling cascade is Ca 2+ /calmodulin-dependent kinase II (CaMKII; for review, Zalcman et al, 2018). The high abundance of CaMKII in dendritic synapses suggests that kinase might participate in establishing the structure of the cytoskeleton in the dendritic spine.…”

Section: Discussionmentioning

confidence: 99%

Early Effects of Aβ Oligomers on Dendritic Spine Dynamics and Arborization in Hippocampal Neurons

Ortiz-Sanz

Gaminde-Blasco

Valero

et al. 2020

Front. Synaptic Neurosci.

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Alzheimer's disease (AD) is a neurodegenerative disorder that leads to impaired memory and cognitive deficits. Spine loss as well as changes in spine morphology correlates with cognitive impairment in this neurological disorder. Many studies in animal models and ex vivo cultures indicate that amyloid β-peptide (Aβ) oligomers induce synaptic damage early during the progression of the disease. Here, in order to determine the events that initiate synaptic alterations, we acutely applied oligomeric Aβ to primary hippocampal neurons and an ex vivo model of organotypic hippocampal cultures from a mouse after targeted expression of EGFP to allow high-resolution imaging and algorithmbased evaluation of spine changes. Dendritic spines were classified as thin, stubby or mushroom, based on morphology. In vivo, time-lapse imaging showed that the three spine types were relatively stable, although their stability significantly decreased after treatment with Aβ oligomers. Unexpectedly, we observed that the density of total dendritic spines increased in organotypic hippocampal slices treated with Aβ compared to control cultures. Specifically, the fraction of stubby spines significantly increased, while mushroom and thin spines remained unaltered. Pharmacological tools revealed that acute Aβ oligomers induced spine changes through mechanisms involving CaMKII and integrin β1 activities. Additionally, analysis of dendritic complexity based on a 3D reconstruction of the whole neuron morphology showed an increase in the apical dendrite length and branching points in CA1 organotypic hippocampal slices treated with Aβ. In contrast to spines, the morphological changes were affected by integrin β1 but not by CaMKII inhibition. Altogether, these data indicate that the Aβ oligomers exhibit early dual effects by acutely enhancing dendritic complexity and spine density.

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Section: Discussionmentioning

confidence: 99%

Early Effects of Aβ Oligomers on Dendritic Spine Dynamics and Arborization in Hippocampal Neurons

Ortiz-Sanz

Gaminde-Blasco

Valero

et al. 2020

Front. Synaptic Neurosci.

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“…Within the cortical neuronal subtypes, 80% can be characterized as excitatory projection neurons and 20% as inhibitory interneurons . Such functional diversity of neurons explains why this network of cortical connectivity is affected in many neuropsychiatric disorders , and the dysfunction of cortical circuitry may account for the cognitive deficits seen in AS mice . Human evolution is characterized by a considerable increase in size and complexity of the prefrontal cortex.…”

Section: Molecular Pathogenesis: the Contribution Of The Hippocampusmentioning

confidence: 99%

“…CaMKII is synthetized in neuronal dendrites and plays a crucial role in learning and memory (for a review, see Ref. ). However, deregulation of CaMKII activity is not exclusive to the cortical structures, being also present in other brain areas, as is further discussed in Cerebellum section.…”

Section: Molecular Pathogenesis: the Contribution Of The Hippocampusmentioning

confidence: 99%

Angelman syndrome: a journey through the brain

et al. 2020

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Angelman syndrome (AS) is an incurable neurodevelopmental disease caused by loss of function of the maternally inherited UBE3A gene. AS is characterized by a defined set of symptoms, namely severe developmental delay, speech impairment, uncontrolled laughter, and ataxia. Current understanding of the pathophysiology of AS relies mostly on studies using the murine model of the disease, although alternative models based on patient-derived stem cells are now emerging. Here, we summarize the literature of the last decade concerning the three major brain areas that have been the subject of study in the context of AS: hippocampus, cortex, and the cerebellum. Our comprehensive analysis highlights the major phenotypes ascribed to the different brain areas. Moreover, we also discuss the major drawbacks of current models and point out future directions for research in the context of AS, which will hopefully lead us to an effective treatment of this condition in humans.

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“…CaMKIIb, a subtype of CaMK II, is widely distributed in the central nervous system. Studies have shown that CaMKIIb is related to cerebral ischemiareperfusion injury and the formation of learning and memory [21,22]. CaMKIIb is one important factor for the neurons physiological activity.…”

Section: Discussionmentioning

confidence: 99%

Roles of CaMKIIβ in the neurotoxicity induced by ropivacaine hydrochloride in dorsal root ganglion

Wen

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Neurotoxicity of local anesthetics is often reported in the clinic, more and more people pay attention to them. CaMKIIb, a subtype of CaMKII, is detected in the central nervous system. Previous study found that CaMKIIb mRNA are up-regulated in DRG neurons treated with ropivacaine hydrochloride, as well as inhibition of Cav3.2 and Cav3.3 expression can improve the local anesthetics neurotoxicity. In this study, we observed the effect of CaMKIIb on neurotoxicity injury induced by ropivacaine hydrochloride with DRG cell in vitro. We first constructed the pAd-shRNA-CaMKIIb-DRG to inhibit CaMKIIb mRNA expression and detected the cell viability, cell apoptosis rate, CaMKIIb, Cav3.2 and Cav3.3 expression. The results showed that ropivacaine hydrochloride caused the DRG cell injury with cell viability decreased and cell apoptosis rate increased, CaMKIIb, Cav3.2 and Cav3.3 expression up-regulated. Interestingly, inhibition of CaMKIIb expression protected the DRG cell from the neurotoxicity injury induced by ropivacaine hydrochloride, increased the cell viability and decreased the apoptosis rate, as well as inhibition of CaMKIIb expression down-regulated Cav3.2 and Cav3.3 expression. In other words, CaMKIIb is involved with the DRG injury induced by ropivacaine hydrochloride. Inhibition CaMKIIb expression improved DRG injury, increased the cell viability and decreased cell apoptosis rate.

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CaMKII Isoforms in Learning and Memory: Localization and Function

Cited by 133 publications

References 127 publications

Early Effects of Aβ Oligomers on Dendritic Spine Dynamics and Arborization in Hippocampal Neurons

Early Effects of Aβ Oligomers on Dendritic Spine Dynamics and Arborization in Hippocampal Neurons

Angelman syndrome: a journey through the brain

Roles of CaMKIIβ in the neurotoxicity induced by ropivacaine hydrochloride in dorsal root ganglion

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