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T-type calcium channels contribute to NMDA receptor-independent synaptic plasticity in hippocampal regular-spiking oriens-alveus interneurons.

Nicholson, E; Kullmann, DM; (2017) T-type calcium channels contribute to NMDA receptor-independent synaptic plasticity in hippocampal regular-spiking oriens-alveus interneurons. The Journal of Physiology , 595 (11) pp. 3449-3458. 10.1113/JP273695. Green open access

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Abstract

NMDA receptor-independent long-term potentiation (LTP) in hippocampal stratum oriens-alveus (O/A) interneurons requires co-activation of postsynaptic group I metabotropic glutamate receptors (mGluRs) and Ca(2+) -permeable AMPA receptors. The rectification properties of such AMPA receptors contribute to the preferential induction of LTP at hyperpolarized potentials. A persistent increase in excitatory transmission can also be triggered by exogenous activation of group I mGluRs while the interneuron is hyperpolarized, or by postsynaptic trains of action potentials in the absence of presynaptic stimulation. Here we identify low-threshold transient (T-type) channels as a further source of Ca(2+) that contributes to synaptic plasticity. T-type Ca(2+) currents were detected in mouse regular-spiking O/A interneurons. Blocking T-type currents pharmacologically prevented LTP induced by high-frequency stimulation of glutamatergic axons, or by application of the group I mGluR agonist dihydroxyphenylglycine (DHPG), paired with postsynaptic hyperpolarization. T-type current blockade also prevented synaptic potentiation induced by postsynaptic action potential trains. Several sources of Ca(2+) thus converge on NMDA receptor-independent LTP induction in O/A interneurons. This article is protected by copyright. All rights reserved.

Type: Article
Title: T-type calcium channels contribute to NMDA receptor-independent synaptic plasticity in hippocampal regular-spiking oriens-alveus interneurons.
Location: England
Open access status: An open access version is available from UCL Discovery
DOI: 10.1113/JP273695
Publisher version: http://dx.doi.org/10.1113/JP273695
Additional information: © 2017 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Experimental Epilepsy
URI: http://discovery.ucl.ac.uk/id/eprint/1540771
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