Glutamate depolarization of glial cells in Necturus optic nerve.
L-Glutamate, 10(-5) to 10(-2) M, depolarized glial cells in the normal and axon-free optic nerve of Necturus by up to 80 mV. The depolarization was maintained if lithium, but not tetramethylammonium, replaced sodium in the bathing solution. It was not blocked by either strophanthidin or tetrodotoxin. The response was accompanied by a membrane conductance increase and was followed by a strophanthidin-sensitive hyperpolarization. These results suggest that the depolarization resulted from sodium entry. D-Glutamate and L-aspartate were less potent but produced a comparable depolarization. gamma-Aminobutyric acid, glycine, taurine or glutamine (up to 10(-3) M) were ineffective.
Tang
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Orkand
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D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D004553:Electric Conductivity; D004594:Electrophysiology; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D008564:Membrane Potentials / Q000187:drug effects; D009338:Necturus maculosus; D009457:Neuroglia / Q000187:drug effects* / Q000502:physiology; D009900:Optic Nerve / Q000187:drug effects* / Q000502:physiology; D013327:Strophanthidin / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D000596:Amino Acids; D005971:Glutamates; D018698:Glutamic Acid; D013779:Tetrodotoxin; D013327:Strophanthidin