Glial Glutamate Receptors

We mainly emphasize the synaptic roles of glutamate receptors expressed by neurons. However, there is increasing evidence that glial glutamate receptors also play physiological roles in the brain (see reviews in refs. 33 and 95). The most direct evidence for activation of glial glutamate receptors by neuronally released glutamate was obtained recently for oligodendrocyte precursor cells in the hippocampus of young and mature rats (96). Schaffer collateral/commissural fiber stimulation led to AMPA receptor-mediated EPSCs in oligodendrocyte precursor cells, which were identified by immunostaining and electron microscopy. Moreover, electron microscopy revealed glutamatergic synapses from boutons onto oligodendrocyte precursor cells that had been physiologically identified and filled with biocytin. The function of the glutamatergic input onto oligodendrocyte precursor cells in vivo is yet unknown. In vitro, glutamate receptor activation of oligodendrocyte precursor cell cultures inhibits their proliferation and maturation into oligodendrocytes (97)

Evidence for mGluR receptor activation by neuronally released glutamate in astrocytes in situ is accumulating. Serveral studies reported a rise of intracellular calcium concentration, calcium waves, or oscillations in astrocytes after electrical stimulations of adjacent nerve fibers (98-100). For example, Schaffer collateral stimulation led to intracellular calcium waves in astrocytes in the stratum radiatum in situ (99). Astrocytic calcium waves appeared to not be a consequence of transient potas sium release from activated neurons, but rather to activation of glial glutamate receptors. First, astrocytic calcium waves could be blocked by an mGluR antagonist, which had a negligible effect on (neuronal) field potentials. Second, the calcium waves were not blocked by the ionotropic glutamate receptor antagonist kynurenate, which blocked the postsynaptic response. Moreover, work from Winder et al. (101) strongly suggests that in the rat hippocampal CA1 region, glia and not neurons contain the metabotropic group II receptor mGluR3 and that the coactivation of group II metabotropic glutamate and P-adrenergic receptors occurs in glia and not in CA1 pyramidal neurons (see Fig. 1).

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