title: Modulation of neostriatal activity by iontophoresis of ascorbic acid.
abstract: Iontophoresis (20-80 nA) of ascorbic acid (AA) accelerated the firing rate of approximately one-third of the neurons tested in the anteromedial neostriatum of anesthetized rats. When administered to neostriatal neurons that were activated by the simultaneous ejection of glutamic acid (GLU), AA excited more than two-thirds of the cells examined, including many that were not excited by AA alone. At ejection currents above 80 nA, AA further increased the activity of some GLU-activated neurons, but suppressed the firing rate of others. Electrochemical quantification of AA ejection during iontophoresis indicated that the concentration of AA at the tip of the recording electrode was within reasonable physiological limits. It is concluded that endogenous AA may modulate neuronal activity in the neostriatum.
authors.forename: T W
authors.initials: TW
authors.lastname: Gardiner
authors.forename: M
authors.initials: M
authors.lastname: Armstrong-James
authors.forename: A W
authors.initials: AW
authors.lastname: Caan
authors.forename: R M
authors.initials: RM
authors.lastname: Wightman
authors.forename: G V
authors.initials: GV
authors.lastname: Rebec
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D003342:Corpus Striatum / Q000187:drug effects*; D004357:Drug Synergism; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D007478:Iontophoresis; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013268:Stimulation, Chemical
chemical_list: D005971:Glutamates; D018698:Glutamic Acid; D001205:Ascorbic Acid