Neuronal activity regulates correlated network properties of spontaneous calcium transients in astrocytes in situ.
Spontaneous neuronal activity is essential to neural development. Until recently, neurons were believed to be the only excitable cells to display spontaneous activity. However, cultured astrocytes and, more recently, astrocytes in situ are now known to exhibit spontaneous Ca2+ transients. Here we used Ca2+ imaging of astrocytes from transgenic mice for the simultaneous monitoring of [Ca2+]i changes in large numbers of astrocytes. We found that spontaneous activity is a common property of most brain astrocytes that is lost in response to a lesion. These spontaneous [Ca2+]i oscillations require extracellular and intracellular Ca2+. Moreover, network analysis revealed that most astrocytes formed correlated networks of dozens of these cells, which were synchronous with both astrocytes and neurons. We found that decreasing spontaneous [Ca2+]i transients in neurons by TTX does not alter the number of active astrocytes, although it impairs their synchronous network activity. Conversely, bicuculline-induced epileptic patterns of [Ca2+]i transients in neurons cause an increase in the number of active astrocytes and in their network synchrony. Furthermore, activation of non-NMDA and NMDA ionotropic glutamate receptors is required to correlate astrocytic networks. These results show that spontaneous activity in astrocytes and neurons is patterned into correlated neuronal/astrocytic networks in which neuronal activity regulates the network properties of astrocytes. This network activity may be essential for neural development and synaptic plasticity.
Aguado
Fernando
F
Department of Cell Biology and Barcelona Science Park, University of Barcelona, Barcelona E-08028, Spain. aguado@medicina.ub.es
Espinosa-Parrilla
Juan F
JF
Carmona
María A
MA
Soriano
Eduardo
E
D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000166:cytology / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002614:Chelating Agents / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics; D049452:Green Fluorescent Proteins; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D066298:In Vitro Techniques; D007424:Intracellular Fluid / Q000378:metabolism; D008164:Luminescent Proteins / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D008959:Models, Neurological; D009010:Monte Carlo Method; D009415:Nerve Net / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D017470:Receptors, Glutamate / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D002121:Calcium Channel Blockers; D002614:Chelating Agents; D005904:Glial Fibrillary Acidic Protein; D008164:Luminescent Proteins; D017470:Receptors, Glutamate; D011993:Recombinant Fusion Proteins; D049452:Green Fluorescent Proteins; D013779:Tetrodotoxin; D002118:Calcium