PDF(Pubmed)
Abstract：
Dendritic spines are the postsynaptic compartments of excitatory synapses, however, a substantial subset of spines additionally receives inhibitory input. In such dually innervated spines (DiSs), excitatory long-term potentiation (LTP) mechanisms are suppressed, but can be enabled by blocking tonic inhibitory GABAB receptor signaling. Here we show that LTP mechanisms at DiSs are also enabled by two other excitatory LTP stimuli. In hippocampal neurons, these chemical LTP (cLTP) stimuli induced robust movement of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) to DiSs. Such synaptic CaMKII accumulation is an essential LTP mechanism at singly innervated spines (SiSs). Indeed, CaMKII accumulation at DiSs was also accompanied by other readouts for successful LTP induction: spine growth and surface insertion of GluA1. Thus, DiSs are capable of the same LTP mechanisms as SiSs, although induction of these mechanism additionally requires either reduced inhibitory signaling or increased excitatory stimulation. This additional regulation may provide further computational control.
摘要：
树突棘是兴奋性突触的突触后隔室，然而,棘刺的实质子集另外接收抑制性输入。在这种双重神经支配的棘(DiSs)中，兴奋性长时程增强(LTP)机制被抑制，但可以通过阻断强直抑制性GABAB受体信号传导来实现。在这里，我们表明DiSs的LTP机制也可以通过另外两个兴奋性LTP刺激来实现。在海马神经元中，这些化学LTP（cLTP）刺激诱导Ca2/钙调蛋白依赖性蛋白激酶II（CaMKII）向DiSs的强烈运动。这种突触CaMKII积累是单神经支配棘（SiSs）的基本LTP机制。的确,DiSs的CaMKII积累还伴随着其他成功的LTP诱导读数：脊柱生长和GluA1的表面插入。因此，DiSs能够与SiSs具有相同的LTP机制，尽管这些机制的诱导还需要减少抑制性信号或增加兴奋性刺激。该附加调节可以提供进一步的计算控制。
