Distinct coincidence detectors govern the corticostriatal spike timing-dependent plasticity
Distinct coincidence detectors govern the corticostriatal spike timing-dependent plasticity
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DOI：
10.1113/jphysiol.2010.188466
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发表时间：
2010-08-15
影响因子：
5.5
通讯作者：
Venance, Laurent
中科院分区：
文献类型：
--
作者：
Fino, Elodie;Paille, Vincent;Venance, Laurent
皮质纹状体投射构成了基底神经节的主要输入，基底神经节是参与程序性学习的相互连接的皮质下核团的集合。因此，皮质纹状体突触的长期可塑性将为基底神经节在学习和记忆中的功能提供基本机制。我们以前曾报道存在一个皮质纹状体的反Hebbian尖峰时间依赖性可塑性（STDP）在突触到纹状体输出神经元，中型多刺神经元。在这里，我们表明，GABA能传输的封锁逆转了皮质纹状体STDP的时间依赖性。我们探讨了参与皮质纹状体STDP的受体和信号传导机制。尽管STDP的经典模型提出NMDA受体作为唯一的符合检测器，但也已证明多个符合检测器的参与。在这里，我们表明，皮质纹状体STDP依赖于不同的符合探测器。具体来说，长时程增强依赖于NMDA受体的激活，而长时程抑制则需要不同的重合检测器：磷脂酶C β（PLC β）和肌醇三磷酸受体（IP 3R）门控钙库。此外，我们发现PLC β激活由I型代谢型谷氨酸受体、1型毒蕈碱受体和电压敏感性钙通道活性控制。PLC β和IP（3）Rs的激活导致由2-花生四烯酰甘油和大麻素CB 1受体介导的强大的逆行内源性大麻素信号传导。有趣的是，相同的巧合探测器支配皮质纹状体的反Hebbian STDP和Hebbian STDP在皮质突触报告。因此，STDP在皮质纹状体突触诱导的LTP和LTD是由独立的信号传导机制介导的，每一个都由不同的重合检测器控制。
Corticostriatal projections constitute the main input to the basal ganglia, an ensemble of interconnected subcortical nuclei involved in procedural learning. Thus, long-term plasticity at corticostriatal synapses would provide a basic mechanism for the function of basal ganglia in learning and memory. We had previously reported the existence of a corticostriatal anti-Hebbian spike timing-dependent plasticity (STDP) at synapses onto striatal output neurons, the medium-sized spiny neurons. Here, we show that the blockade of GABAergic transmission reversed the time dependence of corticostriatal STDP. We explored the receptors and signalling mechanisms involved in the corticostriatal STDP. Although classical models for STDP propose NMDA receptors as the unique coincidence detector, the involvement of multiple coincidence detectors has also been demonstrated. Here, we show that corticostriatal STDP depends on distinct coincidence detectors. Specifically, long-term potentiation is dependent on NMDA receptor activation, while long-term depression requires distinct coincidence detectors: the phospholipase C beta (PLC beta) and the inositol-trisphosphate receptor (IP3R)-gated calcium stores. Furthermore, we found that PLC beta activation is controlled by group-I metabotropic glutamate receptors, type-1 muscarinic receptors and voltage-sensitive calcium channel activities. Activation of PLC beta and IP(3)Rs leads to robust retrograde endocannabinoid signalling mediated by 2-arachidonoyl-glycerol and cannabinoid CB1 receptors. Interestingly, the same coincidence detectors govern the corticostriatal anti-Hebbian STDP and the Hebbian STDP reported at cortical synapses. Therefore, LTP and LTD induced by STDP at corticostriatal synapses are mediated by independent signalling mechanisms, each one being controlled by distinct coincidence detectors.