Differential time-course of slow afterhyperpolarizations and associated Ca2+ transients in rat CA1 pyramidal neurons:: Further dissociation by Ca2+ buffer

被引:21
作者
Jahromi, BS
Zhang, L
Carlen, PL
Pennefather, P [1 ]
机构
[1] Toronto Hosp, Res Inst, Playfair Neurosci Unit, Toronto, ON M5S 2S2, Canada
[2] Univ Toronto, Dept Surg Neurosurg, Toronto, ON M5S 2S2, Canada
[3] Univ Toronto, Dept Med Neurol, Toronto, ON M5S 2S2, Canada
[4] Univ Toronto, Dept Physiol, Toronto, ON M5S 2S2, Canada
[5] Univ Toronto, MRC Grp Nerve Cell & Synapse, Toronto, ON M5S 2S2, Canada
[6] Univ Toronto, Fac Pharm, Toronto, ON M5S 2S2, Canada
基金
英国医学研究理事会;
关键词
Ca2+-dependent K+ current; hippocampal pyramidal neurons; dendritic Ca2+ signals; confocal Ca2+ imaging; slow afterhyperpolarization current; BAPTA;
D O I
10.1016/S0306-4522(98)00203-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Hippocampal neurons exhibit a slow after hyperpolarization following membrane depolarization; this is thought to reflect an underlying Ca2+-dependent K+ current. This current is potentiated by intermediate concentrations (0.1-1.0 mM) of exogenous Ca2+ buffer [Schwindt P. C. et al. (1992) Neuroscience 47, 571-578; Zhang L. et al. (1995) J. Neurophysiol. 74, 2225-2241]. The relationship between the slow afterhyperpolarization and associated Ca2+ transients was investigated in the presence and absence of added exogenous Ca2+ buffer. Slow afterhyperpolarizations and underlying K+ currents were measured using whole-cell patch-clamp recordings from hippocampal CA1 neurons in acute rat brain slices. Inclusion of fluorescent Ca2+ indicators in the patch pipette solution allowed simultaneous measurement of the evoked subcellular Ca2+ transients using a confocal microscope. The peak Ca2+ signal exhibited an incremental increase with each action potential. This increase eventually reached a plateau with increasing numbers of action potentials. suggesting dye saturation with peak Ca2+ concentrations. As the K-D for Ca2+ of the indicator dyes used was between 200 and 300 nM, it is predicted that saturation will occur when the peak Ca2+ signal exceeds 1 mu M. This occurred with fewer action potentials in dendritic vs somatic compartments. Neither compartment exhibited averaged Ca2+ transients matching the slow afterhyperpolarization time-course, dendritic Ca2+ transients being most divergent. Intracellular accumulation of exogenous Ca2+ buffer, tither by inclusion in the patch pipette or by incubation of the brain slice with its membrane-permeable form, caused a prolongation of the slow afterhyperpolarization but not of the somatic Ca2+ transient. The initial rate of decline of the dendritic Ca transient was diminished, but remained faster than that of the slow afterhyperpolarization. We conclude that neither dendritic nor somatic Ca2+ signals match the slow afterhyperpolarization time-course, with this dissociation bring further magnified by addition of exogenous Ca2+ buffer. The implications of this result are discussed. (C) 1998 IBRO. Published by Elsevier Science Ltd.
引用
收藏
页码:719 / 726
页数:8
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