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