Activity-dependent [Ca2+](i) changes in guinea pig vagal motoneurons: Relationship to the slow afterhyperpolarization

被引:33
作者
LasserRoss, N
Ross, WN
Yarom, Y
机构
[1] NEW YORK MED COLL,DEPT PHYSIOL,VALHALLA,NY 10595
[2] HEBREW UNIV JERUSALEM,INST LIFE SCI,DEPT NEUROBIOL,IL-91904 JERUSALEM,ISRAEL
关键词
D O I
10.1152/jn.1997.78.2.825
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Vagal motoneurons in slices from the guinea-pig brain stem were injected with the fluorescent [Ca2+](i) indicators fura-2, furaptra, or Calcium Green-1. Spike-induced fluorescence changes were measured in the soma and dendrites and simultaneously the long-lasting afterhyperpolarization was recorded with a sharp microelectrode in the soma. Na+ spikes or Ca2+ spikes increased [Ca2+](i) (measured as a change in indicator fluorescence) in all locations in the soma and dendrites. Each spike in a train of action potentials caused a step increase in fluorescence of about equal amplitude when nonsaturating indicators were used. Peak changes at all locations occurred at the time of the last action potential. Transients measured with low concentrations of Calcium Green-1 or furaptra had a recovery time constant of similar to 500-1,500 ms in the cell body. The recovery time course was faster in the dendrites than in the soma. The norepinephrine-sensitive, slow afterhyperpolarization (sAHP) had a time to peak of similar to 800 ms and a recovery time constant of 2-5 s, much longer than the recovery time course of the fluorescence changes. Some of these experiments were repeated on pyramidal neurons from the CA1 region of the rat hippocampus with similar results. In both cell types, the data suggest that the time course of neither the rising phase nor the falling phase of the sAHP, nor the underlying conductance, directly reflects the time course of the [Ca2+](i) change. The mechanism connecting the parameters remains unclear. One possibility is that an additional second messenger system is involved.
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页码:825 / 834
页数:10
相关论文
共 49 条
[1]   RANGE OF MESSENGER ACTION OF CALCIUM-ION AND INOSITOL 1,4,5-TRISPHOSPHATE [J].
ALLBRITTON, NL ;
MEYER, T ;
STRYER, L .
SCIENCE, 1992, 258 (5089) :1812-1815
[2]   FURA-2 CALCIUM TRANSIENTS IN FROG SKELETAL-MUSCLE FIBERS [J].
BAYLOR, SM ;
HOLLINGWORTH, S .
JOURNAL OF PHYSIOLOGY-LONDON, 1988, 403 :151-192
[3]   FREQUENCY-DEPENDENT PROPAGATION OF SODIUM ACTION-POTENTIALS IN DENDRITES OF HIPPOCAMPAL CA1 PYRAMIDAL NEURONS [J].
CALLAWAY, JC ;
ROSS, WN .
JOURNAL OF NEUROPHYSIOLOGY, 1995, 74 (04) :1395-1403
[4]   CALCIUM-DEPENDENT POTASSIUM CONDUCTANCE IN GUINEA-PIG OLFACTORY CORTEX NEURONS INVITRO [J].
CONSTANTI, A ;
SIM, JA .
JOURNAL OF PHYSIOLOGY-LONDON, 1987, 387 :173-194
[5]   CALCIUM-BINDING TO FLUORESCENT CALCIUM INDICATORS - CALCIUM GREEN, CALCIUM ORANGE AND CALCIUM CRIMSON [J].
EBERHARD, M ;
ERNE, P .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1991, 180 (01) :209-215
[6]   CALCIUM SIGNALING IN A NARROW SOMATIC SUBMEMBRANE SHELL DURING SYNAPTIC ACTIVITY IN CEREBELLAR PURKINJE NEURONS [J].
EILERS, J ;
CALLEWAERT, G ;
ARMSTRONG, C ;
KONNERTH, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (22) :10272-10276
[7]   CA-2+-ACTIVATED K+ CURRENT INVOLVEMENT IN NEURONAL FUNCTION REVEALED BY INSITU SINGLE-CHANNEL ANALYSIS IN HELIX NEURONS [J].
GOLA, M ;
DUCREUX, C ;
CHAGNEUX, H .
JOURNAL OF PHYSIOLOGY-LONDON, 1990, 420 :73-109
[8]   EVIDENCE FOR 2 TYPES OF AFTERHYPERPOLARIZATION IN CA1 PYRAMIDAL CELLS IN THE HIPPOCAMPUS [J].
GUSTAFSSON, B ;
WIGSTROM, H .
BRAIN RESEARCH, 1981, 206 (02) :462-468
[9]   Ca2+ buffering and action potential-evoked Ca2+ signaling in dendrites of pyramidal neurons [J].
Helmchen, F ;
Imoto, K ;
Sakmann, B .
BIOPHYSICAL JOURNAL, 1996, 70 (02) :1069-1081
[10]   SUBCELLULAR CALCIUM TRANSIENTS VISUALIZED BY CONFOCAL MICROSCOPY IN A VOLTAGE-CLAMPED VERTEBRATE NEURON [J].
HERNANDEZCRUZ, A ;
SALA, F ;
ADAMS, PR .
SCIENCE, 1990, 247 (4944) :858-862