title: Regulation of Ca++ influx into striatal neurons by kainic acid.
abstract: We investigated the mechanisms by which kainic acid (KA) produces increases in [Ca++]i in single striatal neurons in vitro using fura-2-based microfluorimetry. When neurons were depolarized by perfusion with high K+ or veratridine containing solutions, [Ca++]i rose rapidly to a peak and then declined to a lower sustained plateau that persisted as long as the depolarizing stimulus. The peak high K+-induced rise in [Ca++]i occurred at [K+]o greater than 50 mM and the plateau was largest at 30 mM K+. [K+]o that was greater than 70 mM caused the magnitude of the plateau to decrease. Responses to high K+ stimulation were completely dependent on [Ca++]o and presumably represented Ca++ influx. Nitrendipine partially blocked the peak of the high K+-induced response and completely blocked the sustained plateau Ca++ influx. The nitrendipine-resistant portion of the high K+ response could be completely blocked by predepolarization of the cell in Ca++-free solution. KA also produced large increases in [Ca++]i that were abolished on removal of external Ca++. Predepolarization/nitrendipine greatly reduced the effect of lower [KA] (100 microM). However, KA-induced increases in [Ca++]i became increasingly resistant to block of voltage-sensitive Ca++ channels as [KA] rose above 100 microM, indicating a second route of Ca++ entry that may be the KA receptor-gated ionophore. About one-half the responses to KA (100 microM) also displayed a large oscillation. [Ca++]i rose to a peak, fell and then rose again before finally declining to a plateau level. This oscillation was abolished when all external Na+ was replaced by Li+ and may result from alterations in the buffering of [Ca++]i as a result of KA-induced Na+ influx.
authors.affiliation: Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois.
authors.forename: S N
authors.initials: SN
authors.lastname: Murphy
authors.forename: R J
authors.initials: RJ
authors.lastname: Miller
mesh_terms: D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016202:N-Methylaspartate; D011188:Potassium / Q000494:pharmacology; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects; D012964:Sodium / Q000378:metabolism
chemical_list: D015220:Calcium Channels; D005971:Glutamates; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D018698:Glutamic Acid; D016202:N-Methylaspartate; D012964:Sodium; D011188:Potassium; D007608:Kainic Acid; D002118:Calcium