Sourdet Valérie, Russier Michaël, Daoudal Gaël, Ankri Norbert, Debanne Dominique
Neurobiologie des Canaux Ioniques, Institut National de la Santé et de la Recherche Médicale Unité Mixte de Recherche 464, Universitéde la Méditerranée, F-13916 Marseille Cedex 20, France.
J Neurosci. 2003 Nov 12;23(32):10238-48. doi: 10.1523/JNEUROSCI.23-32-10238.2003.
The cellular substrate for memory is generally attributed to long-lasting changes in synaptic strength. We report here that synaptic or pharmacological activation of the metabotropic glutamate receptor subtype 5 (mGluR5) induces long-term potentiation of intrinsic excitability (LTP-IE) in layer V pyramidal neurons. mGluR5-dependent LTP-IE was associated with a persistent reduction of the afterhyperpolarization (AHP) outward current (IAHP), resulting in the potentiation of EPSP-spike coupling. Apamin occluded induction of LTP-IE, indicating that downregulation of small conductance calcium-dependent potassium (SK) channels mediates this process. In addition to the improved reliability of the input-output function, LTP-IE led to increased temporal precision. The induced reduction of IAHP accelerated the rate of membrane depolarization preceding each action potential and subsequently decreased the jitter of the neuronal discharge. We conclude that mGluR5-dependent LTP-IE not only promotes the spread of excitation in the cortical network but also persistently enhances the temporal fidelity of the neuronal message.
记忆的细胞底物通常归因于突触强度的持久变化。我们在此报告，代谢型谷氨酸受体5（mGluR5）的突触或药理学激活可诱导V层锥体神经元内在兴奋性的长期增强（LTP-IE）。mGluR5依赖性LTP-IE与超极化后外向电流（IAHP）的持续减少相关，导致兴奋性突触后电位-动作电位（EPSP-spike）耦合增强。蜂毒明肽可阻断LTP-IE的诱导，表明小电导钙依赖性钾（SK）通道的下调介导了这一过程。除了提高输入-输出功能的可靠性外，LTP-IE还提高了时间精度。IAHP的诱导性降低加速了每个动作电位之前的膜去极化速率，随后降低了神经元放电的抖动。我们得出结论，mGluR5依赖性LTP-IE不仅促进了皮质网络中兴奋的传播，而且持续增强了神经元信息的时间保真度。
