Leroy Felix, Brann David H, Meira Torcato, Siegelbaum Steven A
Department of Neuroscience, Kavli Institute of Brain Science, Columbia University Medical Center, 1051 Riverside Drive, New York, NY, USA.
Department of Neuroscience, Kavli Institute of Brain Science, Columbia University Medical Center, 1051 Riverside Drive, New York, NY, USA.
Neuron. 2017 Aug 30;95(5):1089-1102.e5. doi: 10.1016/j.neuron.2017.07.036. Epub 2017 Aug 17.
Input-timing-dependent plasticity (ITDP) is a circuit-based synaptic learning rule by which paired activation of entorhinal cortical (EC) and Schaffer collateral (SC) inputs to hippocampal CA1 pyramidal neurons (PNs) produces a long-term enhancement of SC excitation. We now find that paired stimulation of EC and SC inputs also induces ITDP of SC excitation of CA2 PNs. However, whereas CA1 ITDP results from long-term depression of feedforward inhibition (iLTD) as a result of activation of CB1 endocannabinoid receptors on cholecystokinin-expressing interneurons, CA2 ITDP results from iLTD through activation of δ-opioid receptors on parvalbumin-expressing interneurons. Furthermore, whereas CA1 ITDP has been previously linked to enhanced specificity of contextual memory, we find that CA2 ITDP is associated with enhanced social memory. Thus, ITDP may provide a general synaptic learning rule for distinct forms of hippocampal-dependent memory mediated by distinct hippocampal regions.
输入时间依赖可塑性（ITDP）是一种基于回路的突触学习规则，通过该规则，内嗅皮质（EC）与海马CA1锥体神经元（PNs）的谢弗侧支（SC）输入的配对激活会产生SC兴奋性的长期增强。我们现在发现，EC和SC输入的配对刺激也会诱导CA2 PNs的SC兴奋性产生ITDP。然而，CA1的ITDP是由于表达胆囊收缩素的中间神经元上CB1内源性大麻素受体激活导致前馈抑制的长期抑制（iLTD）所致，而CA2的ITDP是通过表达小白蛋白的中间神经元上δ-阿片受体的激活导致iLTD所致。此外，虽然CA1的ITDP先前已与情境记忆的特异性增强相关联，但我们发现CA2的ITDP与社交记忆增强有关。因此，ITDP可能为不同海马区域介导的不同形式的海马依赖性记忆提供一种通用的突触学习规则。
