Astrocytes are thought to detect neuronal activity in the form of intracellular calcium elevations; thereby, astrocytes can regulate neuronal excitability and synaptic transmission. Little is known, however, about how the astrocyte calcium signal regulates the activity of neuronal populations. In this study, we addressed this issue using functional multineuron calcium imaging in hippocampal slice cultures. Under normal conditions, CA3 neuronal networks exhibited temporally correlated activity patterns, occasionally generating large synchronization among a subset of cells. The synchronized neuronal activity was correlated with astrocyte calcium events. Calcium buffering by an intracellular injection of a calcium chelator into multiple astrocytes reduced the synaptic strength of unitary transmission between pairs of surrounding pyramidal cells and caused desynchronization of the neuronal networks. Uncaging the calcium in the astrocytes increased the frequency of neuronal synchronization. These data suggest an essential role of the astrocyte calcium signal in the maintenance of basal neuronal function at the circuit level.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221819 | PMC |
http://dx.doi.org/10.1113/jphysiol.2014.272864 | DOI Listing |
Behav Neurol
January 2025
Laboratory of Neurobiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Astrocytes are the primary cell type in the central nervous system, responsible for maintaining the stability of the brain's internal environment and supporting neuronal functions. Researches have demonstrated the close relationship between astrocytes and the pathophysiology and etiology of major depressive disorder. However, the regulatory mechanisms of astrocytes during depression remain unclear.
View Article and Find Full Text PDFActa Physiol (Oxf)
February 2025
Laboratory of Neuroendocrinology-Molecular Cell Physiology, Faculty of Medicine, Institute of Pathophysiology, University of Ljubljana, Ljubljana, Slovenia.
Aim: Octopamine in the Drosophila brain has a neuromodulatory role similar to that of noradrenaline in mammals. After release from Tdc2 neurons, octopamine/tyramine may trigger intracellular Ca signaling via adrenoceptor-like receptors on neural cells, modulating neurotransmission. Octopamine/tyramine receptors are expressed in neurons and glia, but how each of these cell types responds to octopamine remains elusive.
View Article and Find Full Text PDFAt cellular and circuit levels, drug addiction is considered a dysregulation of synaptic plasticity. In addition, dysfunction of the glutamate transporter 1 (GLT-1) in the nucleus accumbens (NAc) has also been proposed as a mechanism underlying drug addiction. However, the cellular and synaptic impact of GLT-1 alterations in the NAc remain unclear.
View Article and Find Full Text PDFCells
December 2024
Neuroscience Institute, Section of Padova, National Research Council (CNR), 35131 Padova, Italy.
Astrocytes from different brain regions respond with Ca elevations to the catecholamine norepinephrine (NE). However, whether this noradrenergic-mediated signaling is present in astrocytes from the ventral tegmental area (VTA), a dopaminergic circuit receiving noradrenergic inputs, has not yet been investigated. To fill in this gap, we applied a pharmacological approach along with two-photon microscopy and an AAV strategy to express a genetically encoded calcium indicator in VTA astrocytes.
View Article and Find Full Text PDFCNS Neurol Disord Drug Targets
January 2025
School of Medicine, Foshan University, Foshan, 528000, China.
Introduction: Neuroinflammation derived from the activation of the microglia is considered a vital pathogenic factor of Alzheimer's Disease (AD). T-006, a tetramethylpyrazine derivative, has been found to alleviate cognitive deficits via inhibiting tau expression and phosphorylation in AD transgenic mouse models. Recently, T-006 has been proven to dramatically decrease the levels of total Amyloid β (Aβ) peptide and Glial Fibrillary Acidic Protein (GFAP) and suppress the expression of ionized calcium binding adaptor molecule-1 (Iba-1) in APP/PS1 mice.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!