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Role of CaM Kinase II in Nervous System
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Role of CaM Kinase II in Nervous System

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 January 2021) | Viewed by 17316

Special Issue Editor

Prof. Dr. Kohji Fukunaga

E-Mail Website
Guest Editor
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aramaki-Aoba Aoba-ku, Sendai 980-8578, Japan
Interests: CaM kinase II; neuronal plasticity; neuronal death

Special Issue Information

Dear Colleagues,

Since Ca2+/calmodulin-dependent protein kinase II (CaMKII) was discovered, the kinase has been established in the essential roles for consolidation and recall memory in rodents. Importantly, de vovo CaMKII mutations in human genome studies have been shown to be associated with intellectual disability and neurodevelopmental disorders. Although the essential roles of GluN and GluA receptors are established to elucidate synaptic long-term potentiation through CaMKII signaling, it is still unclear how de vovo CaMKII mutations elucidate neurodevelopmental abnormality in humans. Many upstream and downstream targets in CaMKII signaling will be abnormally regulated by de novo CaMKII mutations. In addition, it is remains unclear how CaMKII activities are regulated by epigenetic and environmental stress. To rescue and make individual therapeutics for intellectual disability and neurodevelopmental disorders in humans, we should define the precise causative mechanism and diagnosis to create precision medicine targeting for CaMKII. In this Special Issue, you are welcome to propose concepts for synaptic regulation and circuit modulation by CaMKII signaling using molecular biology, brain imaging, molecular genetics, and AI procedure. We also invite topics on how epigenetic and genetic mutations of transcription factors elicit aberrant CaMKII activity related to memory and cognition disturbance in animals. We will make a strong research network to dissolve the problems of intellectual disability and neurodevelopmental disorders in humans in this Special Issue.

Prof. Kohji Fukunaga
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • CaM kinase II
  • neuronal plasticity
  • de vovo CaMKII mutation
  • intellectual disability
  • neurodevelopmental disorders
  • spine morphology
  • precision medicine
  • epigenetic and genetic mutation

Published Papers (4 papers)

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Review

18 pages, 1306 KiB  
Review
The Role of CaMKII and ERK Signaling in Addiction
by Wenbin Jia, Ichiro Kawahata, An Cheng and Kohji Fukunaga
Int. J. Mol. Sci. 2021, 22(6), 3189; https://doi.org/10.3390/ijms22063189 - 20 Mar 2021
Cited by 18 | Viewed by 4624
Abstract
Nicotine is the predominant addictive compound of tobacco and causes the acquisition of dependence through its interactions with nicotinic acetylcholine receptors and various neurotransmitter releases in the central nervous system. The Ca2+/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) [...] Read more.
Nicotine is the predominant addictive compound of tobacco and causes the acquisition of dependence through its interactions with nicotinic acetylcholine receptors and various neurotransmitter releases in the central nervous system. The Ca2+/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) play a pivotal role in synaptic plasticity in the hippocampus. CaMKII is involved in long-term potentiation induction, which underlies the consolidation of learning and memory; however, the roles of CaMKII in nicotine and other psychostimulant-induced addiction still require further investigation. This article reviews the molecular mechanisms and crucial roles of CaMKII and ERK in nicotine and other stimulant drug-induced addiction. We also discuss dopamine (DA) receptor signaling involved in nicotine-induced addiction in the brain reward circuitry. In the last section, we introduce the association of polyunsaturated fatty acids and cellular chaperones of fatty acid-binding protein 3 in the context of nicotine-induced addiction in the mouse nucleus accumbens and provide a novel target for the treatment of drug abuse affecting dopaminergic systems. Full article
(This article belongs to the Special Issue Role of CaM Kinase II in Nervous System)
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20 pages, 811 KiB  
Review
The Emerging Role of LHb CaMKII in the Comorbidity of Depressive and Alcohol Use Disorders
by Chaya Shor, Wanhong Zuo, Jean D. Eloy and Jiang-Hong Ye
Int. J. Mol. Sci. 2020, 21(21), 8123; https://doi.org/10.3390/ijms21218123 - 30 Oct 2020
Cited by 5 | Viewed by 3345
Abstract
Depressive disorders and alcohol use disorders are widespread among the general population and are significant public health and economic burdens. Alcohol use disorders often co-occur with other psychiatric conditions and this dual diagnosis is called comorbidity. Depressive disorders invariably contribute to the development [...] Read more.
Depressive disorders and alcohol use disorders are widespread among the general population and are significant public health and economic burdens. Alcohol use disorders often co-occur with other psychiatric conditions and this dual diagnosis is called comorbidity. Depressive disorders invariably contribute to the development and worsening of alcohol use disorders, and vice versa. The mechanisms underlying these disorders and their comorbidities remain unclear. Recently, interest in the lateral habenula, a small epithalamic brain structure, has increased because it becomes hyperactive in depression and alcohol use disorders, and can inhibit dopamine and serotonin neurons in the midbrain reward center, the hypofunction of which is believed to be a critical contributor to the etiology of depressive disorders and alcohol use disorders as well as their comorbidities. Additionally, calcium/calmodulin-dependent protein kinase II (CaMKII) in the lateral habenula has emerged as a critical player in the etiology of these comorbidities. This review analyzes the interplay of CaMKII signaling in the lateral habenula associated with depressive disorders and alcohol use disorders, in addition to the often-comorbid nature of these disorders. Although most of the CaMKII signaling pathway’s core components have been discovered, much remains to be learned about the biochemical events that propagate and link between depression and alcohol abuse. As the field rapidly advances, it is expected that further understanding of the pathology involved will allow for targeted treatments. Full article
(This article belongs to the Special Issue Role of CaM Kinase II in Nervous System)
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Graphical abstract

17 pages, 3076 KiB  
Review
Coordination between Calcium/Calmodulin-Dependent Protein Kinase II and Neuronal Nitric Oxide Synthase in Neurons
by Shoma Araki, Koji Osuka, Tsuyoshi Takata, Yukihiro Tsuchiya and Yasuo Watanabe
Int. J. Mol. Sci. 2020, 21(21), 7997; https://doi.org/10.3390/ijms21217997 - 27 Oct 2020
Cited by 32 | Viewed by 4544
Abstract
Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is highly abundant in the brain and exhibits broad substrate specificity, thereby it is thought to participate in the regulation of neuronal death and survival. Nitric oxide (NO), produced by neuronal NO synthase (nNOS), is [...] Read more.
Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is highly abundant in the brain and exhibits broad substrate specificity, thereby it is thought to participate in the regulation of neuronal death and survival. Nitric oxide (NO), produced by neuronal NO synthase (nNOS), is an important neurotransmitter and plays a role in neuronal activity including learning and memory processes. However, high levels of NO can contribute to excitotoxicity following a stroke and neurodegenerative disease. Aside from NO, nNOS also generates superoxide which is involved in both cell injury and signaling. CaMKII is known to activate and translocate from the cytoplasm to the post-synaptic density in response to neuronal activation where nNOS is predominantly located. Phosphorylation of nNOS at Ser847 by CaMKII decreases NO generation and increases superoxide generation. Conversely, NO-induced S-nitrosylation of CaMKII at Cys6 is a prominent determinant of the CaMKII inhibition in ATP competitive fashion. Thus, the “cross-talk” between CaMKII and NO/superoxide may represent important signal transduction pathways in brain. In this review, we introduce the molecular mechanism of and pathophysiological role of mutual regulation between CaMKII and nNOS in neurons. Full article
(This article belongs to the Special Issue Role of CaM Kinase II in Nervous System)
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Graphical abstract

15 pages, 1070 KiB  
Review
CaMKIIβ in Neuronal Development and Plasticity: An Emerging Candidate in Brain Diseases
by Olivier Nicole and Emilie Pacary
Int. J. Mol. Sci. 2020, 21(19), 7272; https://doi.org/10.3390/ijms21197272 - 01 Oct 2020
Cited by 24 | Viewed by 4009
Abstract
The calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous and central player in Ca2+ signaling that is best known for its functions in the brain. In particular, the α isoform of CaMKII has been the subject of intense research and it has [...] Read more.
The calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous and central player in Ca2+ signaling that is best known for its functions in the brain. In particular, the α isoform of CaMKII has been the subject of intense research and it has been established as a central regulator of neuronal plasticity. In contrast, little attention has been paid to CaMKIIβ, the other predominant brain isoform that interacts directly with the actin cytoskeleton, and the functions of CaMKIIβ in this organ remain largely unexplored. However, recently, the perturbation of CaMKIIβ expression has been associated with multiple neuropsychiatric and neurodevelopmental diseases, highlighting CAMK2B as a gene of interest. Herein, after highlighting the main structural and expression differences between the α and β isoforms, we will review the specific functions of CaMKIIβ, as described so far, in neuronal development and plasticity, as well as its potential implication in brain diseases. Full article
(This article belongs to the Special Issue Role of CaM Kinase II in Nervous System)
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