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Characterization of a Calcium‐dependent Current Generating a Slow Afterdepolarization of CA3 Pyramidal Cells in Rat Hippocampal Slice Cultures
Author(s) -
Caeser Manfred,
Brown David A.,
Gähwiler Beat H.,
Knöpfel Thomas
Publication year - 1993
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1993.tb00521.x
Subject(s) - depolarization , muscarine , current clamp , voltage clamp , afterdepolarization , biophysics , afterhyperpolarization , chemistry , membrane potential , reversal potential , bursting , electrophysiology , neuroscience , patch clamp , repolarization , muscarinic acetylcholine receptor , receptor , biology , biochemistry
A depolarization‐induced, slowly decaying inward current was examined in slice‐cultured CA3 pyramidal cells by voltage‐clamp techniques and microfluorometric measurements of cytosolic free Ca 2+ concentration ([Ca 2+ ] i ). Action potentials elicited by intracellular injection of short‐lasting (50 – 100 ms) depolarizing current pulses were followed by a slowly decaying afterhyperpolarization (AHP). After switching to voltage‐clamp mode, short‐lasting (50 – 100 ms) depolarizing voltage jumps from –60 mV to between –30 and 0 mV induced a slowly decaying outward aftercurrent (I AHP ) which was depressed by bath application of muscarine (0.5 μM). In the presence of muscarine, the same depolarizations induced a slowly decaying afterdepolarization (ADP) or inward aftercurrent (I ADP )in voltage‐clamp mode. This current was also induced in the presence of trans(±)‐1‐aminc‐1,3‐cyclopenta‐nedicarboxylic acid ( t ‐ACPD, 5 μM), an agonist of metabotropic glutamate receptors, but not in the presence of noradrenalin (5 μM), while both of these agonists depressed I AHP . I ADP was depressed by reducing the external Ca 2+ concentration from 3.8 to 0.5 mM, by external Co 2+ (1 mM) and by external Cd 2+ (10 – 100 μM). Combined voltage‐clamp recordings and microfluorometric measurements of [Ca 2+ ] i using the Ca 2+ indicator fura‐2 revealed that the amplitude of I ADP was correlated with the amplitude of depolarization‐induced Ca 2+ influx, I ADP was absent at membrane potentials < –90 mV, and reached maximal amplitudes at ∼–55 mV. Raising the extracellular K + concentration from 2.7 to 13.5 mM increased the amplitude of I ADP and resulted in a positively directed shift of the apparent reversal potential of I ADP . When the external Na + concentration was reduced from 157 to 33 or 18 mM the current reversed at more negative potentials and was reduced to 40 and 21%, respectively, of control amplitude. Lowering the external Cl ‐ concentration from 159 to 20 mM did not affect I ADP . We conclude that I ADP most likely represents a Ca 2+ ‐activated cation current, rather than a Ca 2+ tail current, or an electrogenic Ca 2+ extrusion current.