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首页> 美国卫生研究院文献>The Journal of Neuroscience >α5GABAA Receptor Activity Sets the Threshold for Long-Term Potentiation and Constrains Hippocampus-Dependent Memory
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α5GABAA Receptor Activity Sets the Threshold for Long-Term Potentiation and Constrains Hippocampus-Dependent Memory

机译：α5GABAA受体活性为长期增强设定阈值并限制海马依赖性记忆

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Synaptic plasticity, which is the neuronal substrate for many forms of hippocampus-dependent learning, is attenuated by GABA type A receptor (GABAAR)-mediated inhibition. The prevailing notion is that a synaptic or phasic form of GABAergic inhibition regulates synaptic plasticity; however, little is known about the role of GABAAR subtypes that generate a tonic or persistent inhibitory conductance. We studied the regulation of synaptic plasticity by α5 subunit-containing GABAARs (α5GABAARs), which generate a tonic inhibitory conductance in CA1 pyramidal neurons using electrophysiological recordings of field and whole-cell potentials in hippocampal slices from both wild-type and null mutant mice for the α5 subunit of the GABAAR (Gabra5−/− mice). In addition, the strength of fear-associated memory was studied. The results showed that α5GABAAR activity raises the threshold for induction of long-term potentiation in a highly specific band of stimulation frequencies (10–20 Hz) through mechanisms that are predominantly independent of inhibitory synaptic transmission. The deletion or pharmacological inhibition of α5GABAARs caused no change in baseline membrane potential or input resistance but increased depolarization during 10 Hz stimulation. The encoding of hippocampus-dependent memory was regulated by α5GABAARs but only under specific conditions that generate moderate but not robust forms of fear-associated learning. Thus, under specific conditions, α5GABAAR activity predominates over synaptic inhibition in modifying the strength of both synaptic plasticity in vitro and certain forms of memory in vivo.
机译：GABA A型受体（GABAAR）介导的抑制作用减弱了突触可塑性，它是许多形式的海马依赖性学习的神经元底物。普遍的观点是，GABA能抑制的突触或阶段性形式调节突触可塑性。然而，对于产生补品或持续抑制性传导的GABAAR亚型的作用了解甚少。我们研究了包含α5亚基的GABAARs（α5GABAARs）对突触可塑性的调节，该蛋白使用野生型和无效突变型小鼠海马切片中场和全细胞电势的电生理记录，在CA1锥体神经元中产生了抑制性电导。 GABAAR（Gabra5 -/-小鼠）的α5亚基。此外，还研究了恐惧相关记忆的强度。结果表明，α5GABAAR活性通过主要独立于抑制性突触传递的机制，在高度特定的刺激频率带（10–20 Hz）中提高了诱导长期增强的阈值。 α5GABAAR的缺失或药理抑制作用不会引起基线膜电位或输入电阻的变化，但会在10 Hz刺激过程中增加去极化作用。海马依赖性记忆的编码受α5GABAAR的调节，但仅在产生中等但不强烈的恐惧相关学习形式的特定条件下。因此，在特定条件下，α5GABAAR活性在修饰突触可塑性在体外和体内某些形式的记忆强度方面均优于突触抑制。

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