title: T-type calcium channels contribute to NMDA receptor independent synaptic plasticity in hippocampal regular-spiking oriens-alveus interneurons.
abstract: Regular-spiking interneurons in the hippocampal stratum oriens exhibit a form of long-term potentiation of excitatory transmission that is independent of NMDA receptors but requires co-activation of Ca2+-permeable AMPA receptors and group I metabotropic glutamate receptors. We show that T-type Ca2+channels are present in such interneurons. Blockade of T-type currents prevents the induction of long-term potentiation, and also interferes with long-lasting potentiation induced either by postsynaptic trains of action potentials or by pairing postsynaptic hyperpolarization with activation of group I metabotropic receptors. Several Ca2+sources thus converge on the induction of NMDA receptor independent synaptic plasticity.
  
  
  
  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 Ca2+-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 at the same time as the interneuron is hyperpolarized, or by postsynaptic trains of action potentials in the absence of presynaptic stimulation. In the present study, we identify low-threshold transient (T-type) channels as a further source of Ca2+that contributes to synaptic plasticity. T-type Ca2+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, paired with postsynaptic hyperpolarization. T-type current blockade also prevented synaptic potentiation induced by postsynaptic action potential trains. Several sources of Ca2+thus converge on NMDA receptor independent LTP induction in O/A interneurons.
authors.affiliation: University College London Institute of Neurology, London, UK.
authors.forename: Elizabeth
authors.identifier: 0000-0003-3893-9243
authors.initials: E
authors.lastname: Nicholson
authors.affiliation: University College London Institute of Neurology, London, UK.
authors.forename: Dimitri M
authors.initials: DM
authors.lastname: Kullmann
mesh_terms: D000200:Action Potentials; D000818:Animals; D020747:Calcium Channels, T-Type / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D007395:Interneurons / Q000378:metabolism* / Q000502:physiology; D017774:Long-Term Potentiation; D008297:Male; D008734:Methoxyhydroxyphenylglycol / Q000031:analogs & derivatives / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D020747:Calcium Channels, T-Type; D016194:Receptors, N-Methyl-D-Aspartate; D008734:Methoxyhydroxyphenylglycol; C010117:3,4-dihydroxyphenylglycol
keywords: calcium channels; interneurons; synaptic plasticity