期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 595, 期 11, 页码 3449-3458出版社
WILEY
DOI: 10.1113/JP273695
关键词
-
资金
- Welcome Trust
- European Research Council
- Wellcome Trust [104033/Z/14/Z] Funding Source: Wellcome Trust
- MRC [MR/L01095X/1, G0501424, G116/147, G0801316] Funding Source: UKRI
- Medical Research Council [MR/L01095X/1, G116/147, G0801316, G0501424] Funding Source: researchfish
- Wellcome Trust [104033/Z/14/Z] Funding Source: researchfish
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据