Disinhibition mediates a form of hippocampal long-term potentiation in area CA1.
Disinhibition mediates a form of hippocampal long-term potentiation in area CA1.
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DOI：
10.1371/journal.pone.0007224
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发表时间：
2009-09-29
期刊：
影响因子：
3.7
通讯作者：
Woodin MA
中科院分区：
文献类型：
--
作者：
Ormond J;Woodin MA
海马体在哺乳动物大脑中的记忆形成中起着中心作用。它编码信息的能力被认为取决于神经元之间突触连接的可塑性。在构成主要海马输出到皮质的锥体神经元中，位于CA1区，突触前CA3锥体神经元的放电产生单突触兴奋性突触后电位（EPSP），随后迅速产生前馈（双突触）抑制性突触后电位（IPSP）。长时程增强（LTP）的单突触突触的突触能输入已成为突触可塑性的主要模型，部分原因是由于其依赖于NMDA受体（NMDARs），所需的空间和时间的学习在完整的动物。利用成年大鼠海马脑片的全细胞记录，我们发现，从CA3到CA1的突触传递的功效可以增强，而无需在海马能输入处诱导经典的LTP。注意不要直接刺激抑制性纤维，我们表明，在前馈抑制性输入的GABA能可塑性的诱导结果在减少分流的兴奋性电流，产生长期增加的Schaffer侧支介导的突触后电位的振幅。与经典的LTP一样，去抑制介导的LTP需要NMDAR激活，这表明主要归因于前者的学习和记忆类型中的作用，并提高了先前未被识别的与记忆缺陷相关的疾病的治疗干预靶点的可能性，以及大脑其他区域中潜在被忽视的LTP表达位点。
The hippocampus plays a central role in memory formation in the mammalian brain. Its ability to encode information is thought to depend on the plasticity of synaptic connections between neurons. In the pyramidal neurons constituting the primary hippocampal output to the cortex, located in area CA1, firing of presynaptic CA3 pyramidal neurons produces monosynaptic excitatory postsynaptic potentials (EPSPs) followed rapidly by feedforward (disynaptic) inhibitory postsynaptic potentials (IPSPs). Long-term potentiation (LTP) of the monosynaptic glutamatergic inputs has become the leading model of synaptic plasticity, in part due to its dependence on NMDA receptors (NMDARs), required for spatial and temporal learning in intact animals. Using whole-cell recording in hippocampal slices from adult rats, we find that the efficacy of synaptic transmission from CA3 to CA1 can be enhanced without the induction of classic LTP at the glutamatergic inputs. Taking care not to directly stimulate inhibitory fibers, we show that the induction of GABAergic plasticity at feedforward inhibitory inputs results in the reduced shunting of excitatory currents, producing a long-term increase in the amplitude of Schaffer collateral-mediated postsynaptic potentials. Like classic LTP, disinhibition-mediated LTP requires NMDAR activation, suggesting a role in types of learning and memory attributed primarily to the former and raising the possibility of a previously unrecognized target for therapeutic intervention in disorders linked to memory deficits, as well as a potentially overlooked site of LTP expression in other areas of the brain.
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影响因子：
5.5
作者：
ABRAHAM, WC;GUSTAFSSON, B;WIGSTROM, H
通讯作者：
WIGSTROM, H
影响因子：
5.5
作者：
Karnup, S;Stelzer, A
通讯作者：
Stelzer, A
影响因子：
2.9
作者：
Kitamura, Akihiko;Ishibashi, Hitoshi;Nabekura, Junichi
通讯作者：
Nabekura, Junichi
影响因子：
5.3
作者：
Campanac, Emilie;Daoudal, Gael;Debanne, Dominique
通讯作者：
Debanne, Dominique
DOI：
10.1523/jneurosci.6000-08.2009
发表时间：
2009-03-11
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Hardie J;Spruston N
通讯作者：
Spruston N