Chronic pain alters cortical and subcortical plasticity, causing enhanced sensory and affective responses to peripheral nociceptive inputs. Previous studies have shown that ketamine had the potential to inhibit abnormally amplified affective responses of single neurons by suppressing hyperactivity in the anterior cingulate cortex (ACC). However, the mechanism of this enduring effect has yet to be understood at the network level. In this study, we recorded local field potentials from the ACC of freely moving rats. Animals were injected with complete Freund’s adjuvant (CFA) to induce persistent inflammatory pain. Mechanical stimulations were administered to the hind paw before and after CFA administration. We found a significant increase in the high-gamma band (60–100 Hz) power in response to evoked pain after CFA treatment. Ketamine, however, reduced the high-gamma band power in response to evoked pain in CFA-treated rats. In addition, ketamine had a sustained effect on the high-gamma band power lasting up to five days after a single dose administration. These results demonstrate that ketamine has the potential to alter maladaptive neural responses in the ACC induced by chronic pain.

中文翻译：

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氯胺酮使大鼠慢性疼痛模型中前扣带回皮层中的高伽马射线能正常化。

慢性疼痛会改变皮质和皮质下的可塑性，导致对周围伤害感受输入的感觉和情感反应增强。先前的研究表明，氯胺酮有可能通过抑制前扣带回皮质（ACC）的过度活跃来抑制单个神经元的异常放大的情感反应。但是，这种持久作用的机制尚未在网络级别上得到理解。在这项研究中，我们记录了自由移动大鼠ACC的局部场电位。给动物注射完全的弗氏佐剂（CFA），以引起持续的炎性疼痛。在给予CFA之前和之后，对后爪进行机械刺激。我们发现，对CFA治疗后诱发的疼痛做出反应，高伽马频带（60–100 Hz）的功率显着增加。但是，氯胺酮 降低了因CFA治疗的大鼠诱发的疼痛而引起的高伽玛谱带功率。此外，氯胺酮对单剂量给药后长达五天的高伽玛谱带功率具有持续作用。这些结果表明，氯胺酮有可能改变由慢性疼痛引起的ACC中适应不良的神经反应。