Neuroscience
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In the brain, astrocytes occupy a key position between vessels and synapses. Among their numerous functions, these glial cells are key partners of neurons during synaptic transmission. Astrocytes detect transmitter release through receptors and transporters at the level of their processes, which are in close proximity to the tow neuronal elements of synapses. ⋯ In the present review we will discuss the implication of mGluR5s as detectors of synaptic transmission. In particular, we will discuss how the functional properties and localization of these receptors permit the detection of the synaptic signal in a defined temporal window and a given spatial area around the synapse. Furthermore, we will review the impact of their activation on synaptic transmission.
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Neurotransmitters released at synapses activate neighboring astrocytes, which in turn, modulate neuronal activity by the release of diverse neuroactive substances that include classical neurotransmitters such as glutamate, GABA or ATP. Neuroactive substances are released from astrocytes through several distinct molecular mechanisms, for example, by diffusion through membrane channels, by translocation via plasmalemmal transporters or by vesicular exocytosis. ⋯ It is proposed that this paucity of Sb2 molecules in astrocytic vesicles may determine the slow secretion. In the present essay we shall overview multiple aspects of vesicular architecture and types of vesicles based on their cargo and dynamics in astroglial cells.
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Brain plays a central role in energy homeostasis continuously integrating numerous peripheral signals such as circulating nutrients, and in particular blood glucose level, a variable that must be highly regulated. Then, the brain orchestrates adaptive responses to modulate food intake and peripheral organs activity in order to achieve the fine tuning of glycemia. More than fifty years ago, the presence of glucose-sensitive neurons was discovered in the hypothalamus, but what makes them specific and identifiable still remains disconnected from their electrophysiological signature. ⋯ Since then, many studies have identified other actors and emphasized the astroglial participation in this mechanism. Growing evidence suggest that astrocytes form a complex network and have to be considered as spatially coordinated and regulated metabolic units. In this review we aim to provide an updated view of the molecular and respective cellular pathways involved in hypothalamic glucose sensing, and their relevance in physiological and pathological states.
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Astrocytes are fundamental for homoeostasis, defence and regeneration of the central nervous system. Loss of astroglial function and astroglial reactivity contributes to the aging of the brain and to neurodegenerative diseases. Changes in astroglia in aging and neurodegeneration are highly heterogeneous and region-specific. ⋯ For instance, in entorhinal and prefrontal cortices astrocytes do not mount gliotic response to emerging β-amyloid deposits. These deficits in reactivity coincide with higher vulnerability of these regions to AD-type pathology. Astroglial morphology and function can be regulated through environmental stimulation and/or medication suggesting that astrocytes can be regarded as a target for therapies aimed at the prevention and cure of neurodegenerative disorders.
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Astrocytes are the largest glial population in the mammalian brain. Astrocytes in the cerebral cortex are reportedly generated from four sources, namely radial glia, progenitors in the subventricular zone (SVZ progenitors), locally proliferating glia, and NG2 glia; it remains an open question, however, as to what extent these four cell types contribute to the substantial increase in astrocytes that occurs postnatally in the cerebral cortex. Here we summarize all possible sources of astrocytes and discuss their roles in this postnatal increase. In particular, we focus on astrocytes derived from local proliferation within the cortex.