The regulated release of transmitters from astrocytes
Research over the past decade has given us novel insights into the diverse roles played by astrocytes in the functioning of numerous processes within the central nervous system (CNS) that have been the focus of several recent reviews (Anderson and Swanson, 2000; Carmignoto, 2000; Hussy et al., 2000; Araque et al., 2001; Haydon, 2001; Mazzanti et al., 2001; Cotrina and Nedergaard, 2002; Chen and Swanson, 2003). This review focuses on recent observations concerning the mechanisms of release of chemical transmitters from astrocytes. Two observations in 1994 led to a significant breakthrough in our thinking about astrocyte function (Nedergaard, 1994; Parpura et al., 1994). These studies showed that calcium elevations in astrocytes could lead to delayed neuronal calcium elevations. However, the mechanisms believed to underlie astrocyte-to-neuron signaling were quite distinct. While Nedergaard concluded that gap junctions mediate astrocyte-to-neuron signaling, Parpura et al. found evidence to support the notion that glutamate released from the astrocyte leads to an N-methyl-D-Aspartate receptor (NMDAR)-dependent elevation of neuronal calcium. Although additional support for the role of gap junctions has come from studies in the locus coeruleus (Alvarez-Maubecin et al., 2000), there is greater evidence to support the concept that it is the extracellular release of chemical transmitters from astrocytes that mediates astrocyte-to-neuron signaling.
KeywordsAtrial Natriuretic Peptide Glutamate Release Spreading Depression Neuronal Signaling Niflumic Acid
Atrial natriuretic peptide
Central nervous system
Excitatory amino acid
R(+)-[(6,7-dichloro-2-cyclopentyl-2,3-dihydro-2-methyl-1-oxo-1 H-inden-5-yl)-oxy]acetic acid
Pyridoxal phosphate-6-azophenyl-2′-4′-disulfonic acid
Intracellular concentration of ion X
- [X±] o
Extracellular concentration of ion X
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