Astrocyte Calcium Signaling Shifts the Polarity of Presynaptic Plasticity

Letellier, Mathieu; Goda, Yukiko

doi:10.1016/j.neuroscience.2023.05.032

Cited by 3 publications

(3 citation statements)

References 59 publications

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“…Glu is an excitatory neurotransmitter that not only regulates synapse formation, but also participates in astrocyte migration, differentiation, and apoptosis and is responsible for learning, memory, behavioral, motor, and sensory functions ( 53 ). Gly and Glu act as co-agonists to induce Glutamatergic N-methyl-D-aspartate (NMDA) excitatory potentials, resulting in enhanced neuroexcitotoxicity ( 54 ). GABA is an inhibitory neurotransmitter responsible for brain development, cognitive activity, and attention formation ( 55 ).…”

Section: Neural Pathwaysmentioning

confidence: 99%

Neuroplasticity of children in autism spectrum disorder

Chen,

Wang,

Zhang

et al. 2024

Front. Psychiatry

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder that encompasses a range of symptoms including difficulties in verbal communication, social interaction, limited interests, and repetitive behaviors. Neuroplasticity refers to the structural and functional changes that occur in the nervous system to adapt and respond to changes in the external environment. In simpler terms, it is the brain’s ability to learn and adapt to new environments. However, individuals with ASD exhibit abnormal neuroplasticity, which impacts information processing, sensory processing, and social cognition, leading to the manifestation of corresponding symptoms. This paper aims to review the current research progress on ASD neuroplasticity, focusing on genetics, environment, neural pathways, neuroinflammation, and immunity. The findings will provide a theoretical foundation and insights for intervention and treatment in pediatric fields related to ASD.

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Section: Neural Pathwaysmentioning

confidence: 99%

Neuroplasticity of children in autism spectrum disorder

Chen,

Wang,

Zhang

et al. 2024

Front. Psychiatry

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“…Heterosynaptic LTD can be induced by the activity-dependent release of adenosine three phosphate (ATP) and adenosine from neurons [ 108 ] and astrocytes [ 28 , 109 , 110 ] that are inhibited by the adenosine receptor antagonist [ 108 , 109 ], and diminished by A1 receptor inactivation [ 109 ]. Astrocytes have been shown to control the polarity of NMDA receptors and adenosine-dependent presynaptic plasticity [ 111 ]. In another study, adenosine reinforced weight dependence of heterosynaptic plasticity and inhibition of adenosine A1 receptors impaired it [ 112 ].…”

Section: Other Mechanisms Of Heterosynaptic Plasticitymentioning

confidence: 99%

Heterosynaptic plasticity-induced modulation of synapses

Kourosh-Arami,

Komaki,

Gholami

et al. 2023

J Physiol Sci

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Plasticity is a common feature of synapses that is stated in different ways and occurs through several mechanisms. The regular action of the brain needs to be balanced in several neuronal and synaptic features, one of which is synaptic plasticity. The different homeostatic processes, including the balance between excitation/inhibition or homeostasis of synaptic weights at the single-neuron level, may obtain this. Homosynaptic Hebbian-type plasticity causes associative alterations of synapses. Both homosynaptic and heterosynaptic plasticity characterize the corresponding aspects of adjustable synapses, and both are essential for the regular action of neural systems and their plastic synapses.In this review, we will compare homo- and heterosynaptic plasticity and the main factors affecting the direction of plastic changes. This review paper will also discuss the diverse functions of the different kinds of heterosynaptic plasticity and their properties. We argue that a complementary system of heterosynaptic plasticity demonstrates an essential cellular constituent for homeostatic modulation of synaptic weights and neuronal activity. Graphical Abstract

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“…Astrocytes are a major subtype of non-neuronal cells that populate all regions of the brain 7 and modulate diverse neuronal functions including neurotransmitter clearance, ionic homeostasis, cerebral blood flow, and synaptic development and plasticity [8][9][10][11][12][13][14][15][16][17][18][19] . These glia cells are electrically quiescent but show robust intracellular calcium dynamics [20][21][22][23] .…”

Section: Introductionmentioning

confidence: 99%

Functional activation of dorsal striatum astrocytes improves movement deficits in hemi-parkinsonian mice

Evans,

Baskar,

Ana Raquel

et al. 2024

Preprint

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Parkinson's disease (PD) is characterized by the degeneration of dopaminergic nigrostriatal inputs, which causes striatal network dysfunction and leads to pronounced motor deficits. Recent evidence highlights astrocytes as a potential local source of striatal network modulation. However, it remains unknown how dopamine loss affects striatal astrocyte activity and whether astrocyte activity regulates behavioral deficits in PD. We addressed these questions by performing astrocyte-specific calcium recordings and manipulations using in vivo fiber photometry and chemogenetics. We find that locomotion elicits astrocyte calcium activity over a slower timescale than neurons. Unilateral dopamine depletion reduced locomotion-related astrocyte responses. Chemogenetic activation facilitated astrocyte activity, and improved asymmetrical motor deficits and open field exploratory behavior in dopamine lesioned mice. Together, our results establish a novel role for functional striatal astrocyte signaling in modulating motor function in PD and highlight non-neuronal targets for potential PD therapeutics.

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Astrocyte Calcium Signaling Shifts the Polarity of Presynaptic Plasticity

Cited by 3 publications

References 59 publications

Neuroplasticity of children in autism spectrum disorder

Neuroplasticity of children in autism spectrum disorder

Heterosynaptic plasticity-induced modulation of synapses

Functional activation of dorsal striatum astrocytes improves movement deficits in hemi-parkinsonian mice

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