Le Roux N, Amar M, Moreau A, Baux G, Fossier P
CNRS, Institut de Neurobiologie Alfred Fessard-FRC2118, Laboratoire de Neurobiologie Cellulaire et Moléculaire-UPR9040, Gif sur Yvette F-91198, France.
Eur J Neurosci. 2008 Jun;27(12):3244-56. doi: 10.1111/j.1460-9568.2008.06288.x.
In the cortex, homeostatic plasticity appears to be a key process for maintaining neuronal network activity in a functional range. This phenomenon depends on close interactions between excitatory and inhibitory circuits. We previously showed that application of a high frequency of stimulation (HFS) protocol in layer 2/3 induces parallel potentiation of excitatory and inhibitory inputs on layer 5 pyramidal neurons, leading to an unchanged excitation/inhibition (E/I) balance. These coordinated long-term potentiations of excitation and inhibition correspond to homeostatic plasticity of the neuronal networks. We showed here, on the rat visual cortex, that blockade (with gabazine) or overactivation (with 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol) of GABA(A) receptors enhanced the E/I balance and prevented the potentiation of excitatory and inhibitory inputs after an HFS protocol. These impairements of the GABAergic transmission led to a long-term depression-like effect after an HFS protocol. We also observed that the blockade of inhibition reduced excitation (by 60%), and conversely, the blockade of excitation decreased inhibition (by 90%). These results support the idea that inhibitory interneurons are critical for recurrent interactions underlying homeostatic plasticity in cortical networks.
在皮质中，稳态可塑性似乎是将神经元网络活动维持在功能范围内的关键过程。这种现象取决于兴奋性和抑制性回路之间的紧密相互作用。我们之前表明，在第2/3层应用高频刺激（HFS）方案可诱导第5层锥体神经元上兴奋性和抑制性输入的平行增强，从而导致兴奋/抑制（E/I）平衡不变。这些兴奋性和抑制性的协同长期增强对应于神经元网络的稳态可塑性。我们在此在大鼠视觉皮质上表明，GABA(A)受体的阻断（用荷包牡丹碱）或过度激活（用4,5,6,7-四氢异恶唑并[5,4-c]吡啶-3-醇）增强了E/I平衡，并在HFS方案后阻止了兴奋性和抑制性输入的增强。这些GABA能传递的损害在HFS方案后导致了类似长期抑制的效应。我们还观察到抑制的阻断降低了兴奋性（降低60%），相反，兴奋的阻断降低了抑制性（降低90%）。这些结果支持了抑制性中间神经元对于皮质网络中稳态可塑性潜在的反复相互作用至关重要的观点。
