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首页> 外文期刊>Neuron >A role for Ca2+ stores in kainate receptor-dependent synaptic facilitation and LTP at mossy fiber synapses in the hippocampus.
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A role for Ca2+ stores in kainate receptor-dependent synaptic facilitation and LTP at mossy fiber synapses in the hippocampus.

机译:Ca2 +储存在海马体苔藓纤维突触中的海藻酸盐受体依赖性突触促进和LTP中的作用。

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摘要

Compared with NMDA receptor-dependent LTP, much less is known about the mechanism of induction of NMDA receptor-independent LTP; the most extensively studied form of which is mossy fiber LTP in the hippocampus. In the present study we show that Ca2+-induced Ca2+ release from intracellular stores is involved in the induction of mossy fiber LTP. This release also contributes to the kainate receptor-dependent component of the pronounced synaptic facilitation that occurs during high-frequency stimulation. We also present evidence that the trigger for this Ca2+ release is Ca2+ permeation through kainate receptors. However, these novel synaptic mechanisms can be bypassed when the Ca2+ concentration is raised (from 2 to 4 mM), via a compensatory involvement of L-type Ca2+ channels. These findings suggest that presynaptic kainate receptors at mossy fiber synapses can initiate a cascade involving Ca2+ release from intracellular stores that is important in both short-term and long-term plasticity.
机译:与NMDA受体依赖性LTP相比,关于NMDA受体依赖性LTP的诱导机制的了解还少得多。研究最广泛的形式是海马中的苔藓纤维LTP。在本研究中,我们表明Ca2 +诱导的Ca2 +从细胞内储存的释放参与了生苔纤维LTP的诱导。这种释放还有助于在高频刺激过程中发生的突触促进作用中的依赖于红藻氨酸受体的成分。我们还提供了证据表明,这种Ca2 +释放的触发因素是Ca2 +通过海藻酸盐受体的渗透。但是,当Ca2 +浓度升高(从2到4 mM)时,可以通过L型Ca2 +通道的补偿参与而绕过这些新的突触机制。这些发现表明,在长满苔藓的纤维突触中的突触前的海藻酸酯受体可以引发级联,涉及从细胞内存储中释放Ca 2+,这对于短期和长期可塑性都很重要。

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