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Spontaneous release from mossy fiber terminals inhibits Ni 2+ ‐sensitive T‐type Ca 2+ channels of CA3 pyramidal neurons in the rat organotypic hippocampal slice
Author(s) -
Reid Christopher A.,
Xu Shenghong,
Williams David A.
Publication year - 2008
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20419
Subject(s) - chemistry , cnqx , depolarization , biophysics , apical dendrite , neuroscience , postsynaptic potential , dendrite (mathematics) , soma , ampa receptor , nmda receptor , biology , biochemistry , geometry , receptor , mathematics
Mossy fibers (axons arising from dentate granule cells) form large synaptic contacts exclusively onto the proximal apical dendrites of CA3 pyramidal neurons. They can generate large synaptic currents that occur in close proximity to the soma. These properties mean that active conductance in the proximal apical dendrite could have a disproportionate influence on CA3 pyramidal neuron excitability. Ni 2+ ‐sensitive T‐type Ca 2+ channels are important modulators of dendritic excitability. Here, we use an optical approach to determine the contribution of Ni 2+ (100 μM)‐sensitive Ca 2+ channels to action potential (AP) elicited Ca 2+ flux in the soma, proximal apical and distal apical dendrites. At resting membrane potentials Ni 2+ ‐sensitive Ca 2+ channels do not contribute to the Ca 2+ signal in the proximal apical dendrite, but do contribute in the other cell regions. Spontaneous release from mossy fiber terminals acting on 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX)‐sensitive postsynaptic channels underlies a tonic inhibition of Ni 2+ ‐sensitive channels. Chelating Zn 2+ with CaEDTA blocks CNQX‐sensitive changes in Ca 2+ flux implicating a mechanistic role of this ion in T‐type Ca 2+ channel block. To test if this inhibition influenced excitability, progressively larger depolarizing pulses were delivered to CA3 pyramidal neurons. CNQX significantly reduced the size of the depolarizing step required to generate APs and increased the absolute number of APs per depolarizing step. This change in AP firing was completely reversed by the addition of Ni 2+ . This mechanism may reduce the impact of T‐type Ca 2+ channels in a region where large synaptic events are common. © 2008 Wiley‐Liss, Inc.

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