Postsynaptic calcium influx at single synaptic contacts between pyramidal neurons and bitufted interneurons in layer 2/3 of rat neocortex is enhanced by backpropagating action potentials
Postsynaptic calcium influx at single synaptic contacts between pyramidal neurons and bitufted interneurons in layer 2/3 of rat neocortex is enhanced by backpropagating action potentials
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DOI：
10.1523/jneurosci.2852-03.2004
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发表时间：
2004-02-11
影响因子：
5.3
通讯作者：
Sakmann, B
中科院分区：
文献类型：
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作者：
Kaiser, KMM;Lübke, J;Sakmann, B
大鼠躯体感觉皮层第2/3层（L2/3）的锥体神经元通过突触兴奋位于同一皮层的生长抑素阳性抑制性双簇状中间神经元。由反向传播动作电位（AP）诱发的体积平均树突[Ca 2 +]（i）的升高通过逆行信号（可能是树突GABA）减少了多巴胺能兴奋。为了测量阈上兴奋期间突触接触处局部[Ca 2 +]（i）的升高，我们在急性切片制备中鉴定了成对的锥体细胞和双簇细胞中的单个突触接触，每个细胞均装载有Ca 2+指示剂染料。在L2/3锥体神经元中诱发的重复AP（50 Hz时10 - 15个AP）在双簇细胞中引起促进单一EPSP。阈下EPSP诱发突触后树突部位[Ca 2 +]（i）瞬时升高，峰值幅度为80 - 250 nM。局部突触后[Ca 2 +]（i）瞬变被限制为类似于10妈妈的树突长度，持续类似于200毫秒，并主要由NMDA受体通道介导。当EPSP为阈上时，诱发的AP反向传播到顶端和基底树突状乔木，并使活性接触处的局部[Ca 2 +]（i）瞬变增加约两倍，峰值幅度达到130 - 450 nM。该值在半最大树突[Ca 2 +]（i）的范围内，引起从锥体的终扣的谷氨酸释放的逆行抑制。突触诱发的反向传播AP在突触接触处局部增强树枝状Ca 2+内流可能代表了一种机制，通过该机制，逆行信号可以限制L2/3锥体重复激活时双簇中间神经元的兴奋。
Pyramidal neurons in layer 2/3 (L2/3) of the rat somatosensory cortex excite somatostatin-positive inhibitory bitufted interneurons located in the same cortical layer via glutamatergic synapses. A rise in volume-averaged dendritic [Ca2+](i) evoked by backpropagating action potentials (APs) reduces glutamatergic excitation via a retrograde signal, presumably dendritic GABA. To measure the rise in local [Ca2+](i) at synaptic contacts during suprathreshold excitation, we identified single synaptic contacts in the acute slice preparation in pairs of pyramidal and bitufted cells each loaded with a Ca2+ indicator dye. Repetitive APs ( 10 - 15 APs at 50 Hz) evoked in a L2/3 pyramidal neuron gave rise to facilitating unitary EPSPs in the bitufted cell. Subthreshold EPSPs evoked a transient rise in [Ca2+](i) of 80 - 250 nM peak amplitude at the postsynaptic dendritic site. The local postsynaptic [Ca2+](i) transient was restricted to similar to 10 mum of dendritic length, lasted for similar to 200 msec, and was mediated predominantly by NMDA receptor channels. When EPSPs were suprathreshold, the evoked AP backpropagated into the apical and basal dendritic arbor and increased the local [Ca2+](i) transient at active contacts by approximately twofold, with a peak amplitude reaching 130 - 450 nM. This value is in the range of the half-maximal dendritic [Ca2+](i), evoking retrograde inhibition of glutamate release from boutons of pyramids. The localized enhancement of dendritic Ca2+ influx at synaptic contacts by synaptically evoked backpropagating APs could represent one mechanism by which a retrograde signal can limit the excitation of bitufted interneurons by L2/3 pyramids when these are repetitively active.