Dataset Information

Functional MRI in mice lacking IP3-dependent calcium signaling in astrocytes.

ABSTRACT: Functional magnetic resonance imaging (fMRI) is a fundamental tool to investigate human brain networks. However, the cellular mechanisms underlying fMRI signals are not fully understood. One hypothetical mechanism is the putative vascular control exerted by cytosolic calcium in perivascular astrocytes. We have performed combined fMRI-electrophysiology experiments in mice lacking the inositol 1,4,5-triphosphate-type-2 receptor, with the primary pathway of cytosolic calcium increase eliminated into astrocytes. Our results show that evoked electrophysiologic activity and fMRI signals acquired during either transient or sustained neuronal activations occur independently of these large calcium signals. This result challenges the suggested intermediary role of astrocytic calcium surges in fMRI-signal generation.

SUBMITTER: Jego P

PROVIDER: S-EPMC4269735 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature

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Functional MRI in mice lacking IP3-dependent calcium signaling in astrocytes.

Jego Pierrick P Pacheco-Torres Jesús J Araque Alfonso A Canals Santiago S

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 20140806 10

Functional magnetic resonance imaging (fMRI) is a fundamental tool to investigate human brain networks. However, the cellular mechanisms underlying fMRI signals are not fully understood. One hypothetical mechanism is the putative vascular control exerted by cytosolic calcium in perivascular astrocytes. We have performed combined fMRI-electrophysiology experiments in mice lacking the inositol 1,4,5-triphosphate-type-2 receptor, with the primary pathway of cytosolic calcium increase eliminated int ...[more]

PMID: 25099754

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Project description:Recent years have witnessed an increasing interest in neuron-glia communication. This interest stems from the realization that glia participate in cognitive functions and information processing and are involved in many brain disorders and neurodegenerative diseases. An important process in neuron-glia communications is astrocyte encoding of synaptic information transfer-the modulation of intracellular calcium (Ca(2+)) dynamics in astrocytes in response to synaptic activity. Here, we derive and investigate a concise mathematical model for glutamate-induced astrocytic intracellular Ca(2+) dynamics that captures the essential biochemical features of the regulatory pathway of inositol 1,4,5-trisphosphate (IP(3)). Starting from the well-known two-variable (intracellular Ca(2+) and inactive IP(3) receptors) Li-Rinzel model for calcium-induced calcium release, we incorporate the regulation of IP(3) production and phosphorylation. Doing so, we extend it to a three-variable model (which we refer to as the ChI model) that could account for Ca(2+) oscillations with endogenous IP(3) metabolism. This ChI model is then further extended into the G-ChI model to include regulation of IP(3) production by external glutamate signals. Compared with previous similar models, our three-variable models include a more realistic description of IP(3) production and degradation pathways, lumping together their essential nonlinearities within a concise formulation. Using bifurcation analysis and time simulations, we demonstrate the existence of new putative dynamical features. The cross-couplings between IP(3) and Ca(2+) pathways endow the system with self-consistent oscillatory properties and favor mixed frequency-amplitude encoding modes over pure amplitude-modulation ones. These and additional results of our model are in general agreement with available experimental data and may have important implications for the role of astrocytes in the synaptic transfer of information.

Dataset Information

Functional MRI in mice lacking IP3-dependent calcium signaling in astrocytes.

Publications

Functional MRI in mice lacking IP3-dependent calcium signaling in astrocytes.

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