Na+-dependent transporters: The backbone of astroglial homeostatic function

Verkhratsky, Alexei; Rose, Christine R.

doi:10.1016/j.ceca.2019.102136

Cited by 45 publications

(33 citation statements)

References 167 publications

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“…Atrophy of perisynaptic processes can substantially modify synaptic transmission. Astrocytes, through a wide array of homeostatic transporters localised in the perisynaptic membrane (Verkhratsky & Rose, 2020), control ionostasis and neurotransmitters in the synaptic cleft and supply neurons with neurotransmitter precursors and energy substrates (Verkhratsky & Nedergaard, 2014). Retraction of astrocytic processes and reduction in astrocytic synaptic coverage can, therefore, impact on synaptic transmission and synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

Astrocyte dystrophy in ageing brain parallels impaired synaptic plasticity

et al. 2021

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Little is known about age‐dependent changes in structure and function of astrocytes and of the impact of these on the cognitive decline in the senescent brain. The prevalent view on the age‐dependent increase in reactive astrogliosis and astrocytic hypertrophy requires scrutiny and detailed analysis. Using two‐photon microscopy in conjunction with 3D reconstruction, Sholl and volume fraction analysis, we demonstrate a significant reduction in the number and the length of astrocytic processes, in astrocytic territorial domains and in astrocyte‐to‐astrocyte coupling in the aged brain. Probing physiology of astrocytes with patch clamp, and Ca2+ imaging revealed deficits in K+ and glutamate clearance and spatiotemporal reorganisation of Ca2+ events in old astrocytes. These changes paralleled impaired synaptic long‐term potentiation (LTP) in hippocampal CA1 in old mice. Our findings may explain the astroglial mechanisms of age‐dependent decline in learning and memory.

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Section: Discussionmentioning

confidence: 99%

Astrocyte dystrophy in ageing brain parallels impaired synaptic plasticity

et al. 2021

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“…Besides its pivotal role for fast electrical signalling based on Na + and/or K + flux through ion channels, the NKA enables secondary-active transport, including the Na + /Ca 2+ exchanger (NCX) or the Na + /H + exchanger (NHE) [ 37 , 49 ] (see Figure 3 ). While these transporters do not consume ATP, a reduction in NKA activity from ATP depletion decreases Na + gradients, and indirectly affects their function.…”

Section: Energy Dependence Of the Tripartite Synapsementioning

confidence: 99%

Dysregulation of Astrocyte Ion Homeostasis and Its Relevance for Stroke-Induced Brain Damage

Putten

Fahlke

Kafitz

et al. 2021

IJMS

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Ischemic stroke is a leading cause of mortality and chronic disability. Either recovery or progression towards irreversible failure of neurons and astrocytes occurs within minutes to days, depending on remaining perfusion levels. Initial damage arises from energy depletion resulting in a failure to maintain homeostasis and ion gradients between extra- and intracellular spaces. Astrocytes play a key role in these processes and are thus central players in the dynamics towards recovery or progression of stroke-induced brain damage. Here, we present a synopsis of the pivotal functions of astrocytes at the tripartite synapse, which form the basis of physiological brain functioning. We summarize the evidence of astrocytic failure and its consequences under ischemic conditions. Special emphasis is put on the homeostasis and stroke-induced dysregulation of the major monovalent ions, namely Na+, K+, H+, and Cl-, and their involvement in maintenance of cellular volume and generation of cerebral edema.

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“…In particular, atrophy of perisynaptic processes can substantially modify synaptic transmission. Astrocytes, through a wide array of homeostatic transporters localised in the perisynaptic membrane (Verkhratsky and Rose, 2020), control ionostasis and neurotransmitters in the synaptic cleft and supply neurons with neurotransmitter precursors and energy substrates (Verkhratsky and Nedergaard, 2014). Retraction of astrocytic processes and reduction in astrocytic synaptic coverage can, therefore, impact on synaptic transmission and synaptic plasticity.…”

Section: Reduced Astrocytic Synaptic Coverage Parallels Impaired Synamentioning

confidence: 99%

Astrocytes dystrophy in ageing brain parallels impaired synaptic plasticity

Popov

Brazhe

Denisov³

et al. 2020

Preprint

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Little is known about age-dependent changes in structure and function of astrocytes and of the impact of these into the cognitive decline in the senescent brain. The prevalent view on age-dependent increase in reactive astrogliosis and astrocytic hypertrophy requires scrutiny and detailed analysis. Using two-photon microscopy in conjunction with 3D reconstruction, Sholl and volume fraction analysis we demonstrate a significant reduction in the number and the length of astrocytic processes, in astrocytic territorial domains and in astrocyte-to-astrocyte coupling in the aged brain. Probing physiology of astrocytes with patch-clamp and Ca2+ imaging revealed deficits in K+ and glutamate clearance, and spatiotemporal reorganization of Ca2+ events in old astrocytes. These changes paralleled impaired synaptic long-term potentiation (LTP) in hippocampal CA1 in old mice. Our findings may explain astroglial mechanisms of age-dependent decline in learning and memory.

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Na+-dependent transporters: The backbone of astroglial homeostatic function

Cited by 45 publications

References 167 publications

Astrocyte dystrophy in ageing brain parallels impaired synaptic plasticity

Astrocyte dystrophy in ageing brain parallels impaired synaptic plasticity

Dysregulation of Astrocyte Ion Homeostasis and Its Relevance for Stroke-Induced Brain Damage

Astrocytes dystrophy in ageing brain parallels impaired synaptic plasticity

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