Astrocytic Calcium and cAMP in Neurodegenerative Diseases

Sobolczyk, Marta; Boczek, Tomasz

doi:10.3389/fncel.2022.889939

Cited by 23 publications

(16 citation statements)

References 183 publications

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“…2021 ). The concentration of PDE4D in PAPS would be consistent with the known role of cAMP signaling in promoting calcium signaling in astrocytes ( Sobolczyk and Boczek 2022 ).…”

Section: Resultssupporting

confidence: 74%

Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease

Datta,

Perone,

Morozov

et al. 2023

Cerebral Cortex

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Alzheimer’s disease cortical tau pathology initiates in the layer II cell clusters of entorhinal cortex, but it is not known why these specific neurons are so vulnerable. Aging macaques exhibit the same qualitative pattern of tau pathology as humans, including initial pathology in layer II entorhinal cortex clusters, and thus can inform etiological factors driving selective vulnerability. Macaque data have already shown that susceptible neurons in dorsolateral prefrontal cortex express a “signature of flexibility” near glutamate synapses on spines, where cAMP-PKA magnification of calcium signaling opens nearby potassium and hyperpolarization-activated cyclic nucleotide-gated channels to dynamically alter synapse strength. This process is regulated by PDE4A/D, mGluR3, and calbindin, to prevent toxic calcium actions; regulatory actions that are lost with age/inflammation, leading to tau phosphorylation. The current study examined whether a similar “signature of flexibility” expresses in layer II entorhinal cortex, investigating the localization of PDE4D, mGluR3, and HCN1 channels. Results showed a similar pattern to dorsolateral prefrontal cortex, with PDE4D and mGluR3 positioned to regulate internal calcium release near glutamate synapses, and HCN1 channels concentrated on spines. As layer II entorhinal cortex stellate cells do not express calbindin, even when young, they may be particularly vulnerable to magnified calcium actions and ensuing tau pathology.

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“…2021 ). The concentration of PDE4D in PAPS would be consistent with the known role of cAMP signaling in promoting calcium signaling in astrocytes ( Sobolczyk and Boczek 2022 ).…”

Section: Resultssupporting

confidence: 74%

Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease

Datta,

Perone,

Morozov

et al. 2023

Cerebral Cortex

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“…Neuron-astrocyte communication primarily occurs through G-protein coupled receptors (GPCRs) on astrocytes ( Kofuji and Araque, 2021 ). GPCR activation leads to downstream signaling cascades, which includes the phospholipase C (PLC)/inositol 1,4,5-triphosphate (IP3) pathway, resulting in calcium release from the endoplasmic reticulum ( Agulhon et al, 2008 ; Sobolczyk and Boczek, 2022 ). The increase of calcium influences the release of gliotransmitters like ATP, D-serine, and glutamate, which then exert their effects on neurons ( Parpura et al, 1994 ; Halassa and Haydon, 2010 ; Sild and Van Horn, 2013 ; Pirttimaki et al, 2017 ).…”

Section: Microcircuit Determinants Of Repetitive Behaviormentioning

confidence: 99%

Striatal insights: a cellular and molecular perspective on repetitive behaviors in pathology

Burton,

Longaretti,

Zlatanovic

et al. 2024

Front. Cell. Neurosci.

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Animals often behave repetitively and predictably. These repetitive behaviors can have a component that is learned and ingrained as habits, which can be evolutionarily advantageous as they reduce cognitive load and the expenditure of attentional resources. Repetitive behaviors can also be conscious and deliberate, and may occur in the absence of habit formation, typically when they are a feature of normal development in children, or neuropsychiatric disorders. They can be considered pathological when they interfere with social relationships and daily activities. For instance, people affected by obsessive-compulsive disorder, autism spectrum disorder, Huntington’s disease and Gilles de la Tourette syndrome can display a wide range of symptoms like compulsive, stereotyped and ritualistic behaviors. The striatum nucleus of the basal ganglia is proposed to act as a master regulator of these repetitive behaviors through its circuit connections with sensorimotor, associative, and limbic areas of the cortex. However, the precise mechanisms within the striatum, detailing its compartmental organization, cellular specificity, and the intricacies of its downstream connections, remain an area of active research. In this review, we summarize evidence across multiple scales, including circuit-level, cellular, and molecular dimensions, to elucidate the striatal mechanisms underpinning repetitive behaviors and offer perspectives on the implicated disorders. We consider the close relationship between behavioral output and transcriptional changes, and thereby structural and circuit alterations, including those occurring through epigenetic processes.

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“…Even though this review focused primarily on neurons, it is important to point out that glial cells, such as astrocytes and microglia, also play crucial roles in epilepsy and neurodegenerative diseases as highlighted in many excellent reviews on this topic ( Salter and Stevens, 2017 ; Patel et al, 2019 ; Santello et al, 2019 ; Escartin et al, 2021 ). Equally important is that Ca 2+ signaling and mitochondria Ca 2+ transport play crucial roles in these cells in the context of many neurological diseases ( Shigetomi et al, 2019 ; Lim et al, 2021b ; Heuser and Enger, 2021 ; Sobolczyk and Boczek, 2022 ). Thus, another task for future studies would be to define cell-type specific roles of MCU and other molecular components of mitochondrial Ca 2+ transport in neurological diseases by genetically targeting these molecules in neurons, glia, and immune cells.…”

Section: Mitochondrial Ca 2+ Cycling In Neurologic...mentioning

confidence: 99%

Mitochondrial calcium cycling in neuronal function and neurodegeneration

Walters

Usachev

2023

Front. Cell Dev. Biol.

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Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca2+) buffering, and apoptotic signaling. In neurons, Ca2+ buffering is particularly important as it helps to shape Ca2+ signals and to regulate numerous Ca2+-dependent functions including neuronal excitability, synaptic transmission, gene expression, and neuronal toxicity. Over the past decade, identification of the mitochondrial Ca2+ uniporter (MCU) and other molecular components of mitochondrial Ca2+ transport has provided insight into the roles that mitochondrial Ca2+ regulation plays in neuronal function in health and disease. In this review, we discuss the many roles of mitochondrial Ca2+ uptake and release mechanisms in normal neuronal function and highlight new insights into the Ca2+-dependent mechanisms that drive mitochondrial dysfunction in neurologic diseases including epilepsy, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. We also consider how targeting Ca2+ uptake and release mechanisms could facilitate the development of novel therapeutic strategies for neurological diseases.

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Astrocytic Calcium and cAMP in Neurodegenerative Diseases

Cited by 23 publications

References 183 publications

Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease

Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease

Striatal insights: a cellular and molecular perspective on repetitive behaviors in pathology

Mitochondrial calcium cycling in neuronal function and neurodegeneration

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