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An I d ‐like current that is downregulated by Ca 2+ modulates information coding at CA3–CA3 synapses in the rat hippocampus
Author(s) -
Saviane Chiara,
Mohajerani Majid H.,
Cherubini Enrico
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2003.00513.x
Subject(s) - neuroscience , hippocampus , current (fluid) , biology , coding (social sciences) , chemistry , physics , statistics , mathematics , thermodynamics
Voltage‐gated K + channels localised on presynaptic nerve terminals control information coding by modulating presynaptic firing and synaptic efficacy in target neurones. We found that at CA3–CA3 connections in hippocampal slice cultures, a fast‐activating, slowly inactivating K + conductance similar to the so‐called delay current ( I D ) is responsible for the delayed appearance of the first spike upon membrane depolarisation, for action potential repolarisation and for modulation of transmitter release. The I d ‐like current was downregulated by intracellular Ca 2+ , as indicated by the increased delay in the appearance of the first action potential following either the block of Ca 2+ flux through voltage‐dependent Ca 2+ channels with Cd 2+ or replacement of the bathing solution with one devoid of Ca 2+ . In both cases, this effect was reversed by blocking this conductance with a low concentration of 4‐aminopyridine (4‐AP, 10‐50 μM). Application of 4‐AP shortened the delay to the first spike generation, prevented the effect of Cd 2+ and increased the spike duration. The earlier appearance of the first action potential was also observed in the presence of dendrotoxin‐1 (100 nM). In voltage‐clamp experiments larger currents were recorded in the absence of extracellular Ca 2+ , thus confirming the downregulation of the I d ‐like current by Ca 2+ due to the positive shift of its inactivation. Spike broadening was associated with an enhancement of synaptic efficacy in target neurones, as assessed by the increase in EPSC amplitude and in the percentage of successes. Moreover, in the presence of 4‐AP, EPSCs appeared with a longer latency and were more scattered. This conductance is therefore crucial for setting the timing and strength of synaptic transmission at CA3–CA3 connections. It is conceivable that switching off I D by increasing intracellular Ca 2+ following activity‐dependent processes may facilitate network synchronisation and crosstalk between CA3 pyramidal cells, leading to seizure activity.