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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

Spontaneous release from mossy fiber terminals inhibits Ni 2+ ‐sensitive T‐type Ca 2+ channels of... 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. Ni2+‐sensitive T‐type Ca2+ channels are important modulators of dendritic excitability. Here, we use an optical approach to determine the contribution of Ni2+ (100 μM)‐sensitive Ca2+ channels to action potential (AP) elicited Ca2+ flux in the soma, proximal apical and distal apical dendrites. At resting membrane potentials Ni2+‐sensitive Ca2+ channels do not contribute to the Ca2+ 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 Ni2+‐sensitive channels. Chelating Zn2+ with CaEDTA blocks CNQX‐sensitive changes in Ca2+ flux implicating a mechanistic role of this ion in T‐type Ca2+ 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 Ni2+. This mechanism may reduce the impact of T‐type Ca2+ channels in a region where large synaptic events are common. © 2008 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

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

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References (48)

Publisher
Wiley
Copyright
Copyright © 2008 Wiley‐Liss, Inc.
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/hipo.20419
pmid
18306285
Publisher site
See Article on Publisher Site

Abstract

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. Ni2+‐sensitive T‐type Ca2+ channels are important modulators of dendritic excitability. Here, we use an optical approach to determine the contribution of Ni2+ (100 μM)‐sensitive Ca2+ channels to action potential (AP) elicited Ca2+ flux in the soma, proximal apical and distal apical dendrites. At resting membrane potentials Ni2+‐sensitive Ca2+ channels do not contribute to the Ca2+ 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 Ni2+‐sensitive channels. Chelating Zn2+ with CaEDTA blocks CNQX‐sensitive changes in Ca2+ flux implicating a mechanistic role of this ion in T‐type Ca2+ 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 Ni2+. This mechanism may reduce the impact of T‐type Ca2+ channels in a region where large synaptic events are common. © 2008 Wiley‐Liss, Inc.

Journal

Hippocampus – Wiley

Published: Jul 1, 2008

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