1995
DOI: 10.1152/jn.1995.73.2.515
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Suppression of a Ca2+ current by NMDA and intracellular Ca2+ in acutely isolated hippocampal neurons

Abstract: 1. Ca2+ current was examined in acutely isolated hippocampal cells with the use of whole cell voltage-clamp recording and under continuous intracellular perfusion. A persistent Ca2+ current was activated by depolarization to -10 mV from a holding potential of -50 mV. 2. The persistent Ca2+ current was suppressed upon a wash out of the intracellular Mg(2+)-ATP. Adenosine 3',5'-cyclic monophosphate (cAMP) introduced intracellularly potentiated the Ca2+ current, and kinase A inhibitor blocked the current. 3. Reve… Show more

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Cited by 10 publications
(4 citation statements)
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“…Neurons were prepared according to the Kay and Wong (1986) method, with the following modifications to increase the harvest of healthy neurons and preserve NMDA responses. Hippocampal slices were prepared by vibratome instead of tissue chopper, the [Ca 2ϩ ] in the incubation solution was reduced to 0.5 mM and the [Mg 2ϩ ] was increased to 7 mM, and 12-15 M CPP (Tocris Cookson, St. Louis) was added during trypsin incubation of tissue slices to preserve the NMDA response (Chen and Wong, 1995a). Healthy neurons were selected for our experiments by choosing those that were uniformly bright under phase-contrast microscopy.…”
Section: Methodsmentioning
confidence: 99%
“…Neurons were prepared according to the Kay and Wong (1986) method, with the following modifications to increase the harvest of healthy neurons and preserve NMDA responses. Hippocampal slices were prepared by vibratome instead of tissue chopper, the [Ca 2ϩ ] in the incubation solution was reduced to 0.5 mM and the [Mg 2ϩ ] was increased to 7 mM, and 12-15 M CPP (Tocris Cookson, St. Louis) was added during trypsin incubation of tissue slices to preserve the NMDA response (Chen and Wong, 1995a). Healthy neurons were selected for our experiments by choosing those that were uniformly bright under phase-contrast microscopy.…”
Section: Methodsmentioning
confidence: 99%
“…In the NG 108 -15 cell line, overexpression of PP2B reduced N-type currents, and this reduction could be overcome by FK-506 (292). Calcium-dependent dephosphorylation of neuronal channels may also be involved in several other studies using OA (59,256,315,466), where channel stimulation was mimicked by calmodulin antagonists or impeded by Ca 2ϩ , respectively. Because the OA concentrations used here were in the micromolar range, it is impossible to tell whether a PP2B has been nonselectively inhibited here by the toxin or whether PP1 was involved indirectly (e.g., through PP2B-mediated dephosphorylation of endogenous PP1 inhibitors).…”
Section: Non-l-type Ca 2ϩ Channelsmentioning
confidence: 99%
“…The regulatory sites consist of a neurotransmitter-binding region with sites for agonists (glutamate) and antagonists, an ion channel which in its open state binds MK-801, a voltage-dependent Mg 2+ -binding site, a regulatory or coactivator site which binds glycine, an inhibitory divalent cation site that binds Zn 2+ , a redox site, and a polyamine (spermine) binding site [7,10]. The NMDA receptor ion channel gates Na + , K + and Ca 2+ ions and in the resting state is blocked in a voltage-dependent manner by Mg 2+ [11,12]. The release of excitatory amino acids during hypoxia activates the NMDA receptor which increases intracellular Ca 2+ [13]; therefore, excessive activation of the NMDA receptor/ion channel complex is an important factor in the cellular brain damage caused by hypoxia/ischemia [14].…”
Section: Introductionmentioning
confidence: 99%