Opera Medica et Physiologica

Astrocyte

Modeling the Role of the Astrocyte Syncytium and K+ Buffering in Maintaining Neuronal Firing Patterns

Introduction
 
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PDF icon omp2019.001.0063.pdf3.65 MB

Abstract

Computational models for two neuron/astrocyte networks are developed to explore mechanisms underlying the astrocytes’ role in maintaining neuronal firing patterns. For the first network, a single neuron receives periodic excitatory inputs at varying frequencies. We consider the role played by several astrocytic dendritic processes, including the Na+-K+ ATPase pump, K+  channels and gap junctions in maintaining extracellular ion homeostasis so that the neuron can faithfully sustain spiking in response to the excitatory input. The second network includes two neurons coupled through mutual inhibitory synapses. Here we consider the role of astrocytic dendritic processes in maintaining anti-phase or synchronous oscillations. Dynamical systems methods, including bifurcation theory and fast/slow analysis, is used to systematically reduce the complex model to a simpler set of equations. In particular, the first network, consisting of differential equations for the neuron and astrocyte membrane potentials, channel state variables and intracellular and extracellular Na+ and K+ concentrations, is reduced to a one dimensional map. Fixed points of the map determine whether the astrocyte can maintain extracellular K+ homeostasis so the neuron can respond to periodic input. 

 

Differential Contribution of GLAST and GLT-1 to Network Sodium Signaling in the Early Postnatal Hippocampus

Introduction

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PDF icon omp2017.003.0048.pdf7.7 MB

Abstract

Recurrent epileptiform activity induces network sodium oscillations in the juvenile hippocampus. In CA1 pyramidal neurons, these oscillations are mainly caused by opening of glutamate-gated ion channels, while in astrocytes, sodium increases are due to sodium-dependent glutamate uptake. Astrocytes express the glutamate transporters GLAST and GLT- 1, which exhibit differential expression patterns during postnatal development. The specific contribution of these transporter subtypes to sodium oscillations is not known. We addressed this question by performing somatic sodium imaging in hippocampal tissue slices from neonatal (postnatal days (P) 2-4) and two-week-old (P14-16) mice. We found that perfusion with Mg2+-free, bicuculline-containing saline caused sodium oscillations in both developmental stages. Moreover, at both P2-4 and P14-16, application of TFB-TBOA to inhibit GLAST and GLT-1 generated fast sodium loading of neurons and termination of oscillatory activity, accompanied by loss of membrane integrity of neurons, while astrocytes experienced only minor increases in baseline sodium. DHK, a GLT-1-specific blocker, induced moderate sodium loading of neurons, reduced the amplitude of neuronal sodium oscillations and increased the oscillation frequency in two-week-old mice. In neonatal animals, DHK increased baseline sodium and reduced the peak amplitude of sodium transients as well, but exerted only moderate effects on network activity. Taken together, our experiments demonstrate the essential role of glutamate uptake for sodium homeostasis and neural function already in the early neonatal brain. Moreover, they suggest that, although GLAST dominates in neonatal tissue and GLT-1 is predominant at P14-16, both transporter subtypes functionally contribute to glutamate clearance during the first three weeks after birth. 

 

Ionic Signalling in Neuronal-Astroglial Interactions

Astroglial excitability

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PDF icon OMP_2016_02_0030.pdf457.26 KB

Abstract

The name astroglia unifies many non-excitable neural cells that act as primary homeostatic cells in the nervous system. Neuronal activity triggers multiple homeostatic responses of astroglia that include increase in metabolic activity and synthesis of neuronal preferred energy substrate lactate, clearance of neurotransmitters and buffering of extracellular K+ ions to name but a few. Many (if not all) of astroglial homeostatic responses are controlled by dynamic changes in the cytoplasmic concentration of two cations, Ca2+ and Na+. Intracellular concentration of these ions is tightly controlled by several transporters and can be rapidly affected by activation of respective fluxes through ionic channels or ion exchangers. Here we provide a comprehensive review of astroglial Ca2+ and Na+ signalling.

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