Power John M, Sah Pankaj
Translational Neuroscience Facility and Department of Physiology, School of Medical Sciences, The University of New South Wales, Sydney, New South Wales, Australia; and Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia
Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.
J Neurophysiol. 2014 Oct 1;112(7):1616-27. doi: 10.1152/jn.00770.2013. Epub 2014 Jun 18.
Glutamatergic synapses on pyramidal neurons are formed on dendritic spines where glutamate activates ionotropic receptors, and calcium influx via N-methyl-d-aspartate receptors leads to a localized rise in spine calcium that is critical for the induction of synaptic plasticity. In the basolateral amygdala, activation of metabotropic receptors is also required for synaptic plasticity and amygdala-dependent learning. Here, using acute brain slices from rats, we show that, in basolateral amygdala principal neurons, high-frequency synaptic stimulation activates metabotropic glutamate receptors and raises spine calcium by releasing calcium from inositol trisphosphate-sensitive calcium stores. This spine calcium release is unevenly distributed, being present in proximal spines, but largely absent in more distal spines. Activation of metabotropic receptors also generated calcium waves that differentially invaded spines as they propagated toward the soma. Dendritic wave invasion was dependent on diffusional coupling between the spine and parent dendrite which was determined by spine neck length, with waves preferentially invading spines with short necks. Spine calcium is a critical trigger for the induction of synaptic plasticity, and our findings suggest that calcium release from inositol trisphosphate-sensitive calcium stores may modulate homosynaptic plasticity through store-release in the spine head, and heterosynaptic plasticity of unstimulated inputs via dendritic calcium wave invasion of the spine head.
锥体神经元上的谷氨酸能突触形成于树突棘上，谷氨酸在此激活离子型受体，通过N-甲基-D-天冬氨酸受体的钙内流导致树突棘钙的局部升高，这对突触可塑性的诱导至关重要。在基底外侧杏仁核中，代谢型受体的激活对于突触可塑性和杏仁核依赖性学习也是必需的。在此，我们使用大鼠的急性脑片表明，在基底外侧杏仁核的主要神经元中，高频突触刺激激活代谢型谷氨酸受体，并通过从三磷酸肌醇敏感的钙库中释放钙来提高树突棘钙水平。这种树突棘钙释放分布不均，存在于近端树突棘中，但在更远端的树突棘中基本不存在。代谢型受体的激活还产生了钙波，这些钙波在向胞体传播时以不同方式侵入树突棘。树突波的侵入依赖于树突棘与母树突之间的扩散耦合，这由树突棘颈部长度决定，波优先侵入颈部短的树突棘。树突棘钙是突触可塑性诱导的关键触发因素，我们的研究结果表明，从三磷酸肌醇敏感的钙库中释放钙可能通过树突棘头部的钙库释放来调节同突触可塑性，并通过树突棘头部的树突钙波侵入来调节未受刺激输入的异突触可塑性。
