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Abstract: The evolution of the central nervous system (CNS) resulted in an appearance of highly specialised neuronal networks optimised for rapid information transfer. In the course of this specialisation neuronal cells lost their metabolic independence and the ability to survive in the absence of homeostatic systems. These homeostatic systems, represented by neuroglia regulate all aspects of CNS function in physiological and pathological conditions. The neurological diseases should be therefore considered as primary gliopathologies, which determine the progression and outcome of neuropathological process. Glial function is intimately regulated by cellular calcium signalling that underlies the specific form of “glial calcium excitability”. Glial Ca2+ signals are triggered by activation of multiple receptors, and are primarily driven by Ca2+ release from the endoplasmic reticulum. In this review we summarise the role of glial calcium signalling in various forms of pathological processes including neurological and psychiatric disorders and neurodegeneration. [Copyright &y& Elsevier]

Exogenous kainate receptor agonists have been shown to modulate inhibitory synaptic transmission in the hippocampus, but the pathways involved in physiological activation of the receptors remain largely unknown. Accumulating evidence indicates that astrocytes can release glutamate in a Ca2+dependent manner and signal to neighboring neurons. They tested the hypothesis that astrocyte-derived glutamate activates kainate receptors on hippocampal interneurons. They reported that elevation of intracellular Ca2+ in astrocytes, induced by uncaging Ca2+ o-nitrophenyl-EGTA, increased action potential-driven spontaneous inhibitory postsynaptic currents in nearby interneurons in rat hippocampal slices.