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首页> 美国卫生研究院文献>Frontiers in Synaptic Neuroscience >Intravascular Ketamine Increases Theta-Burst but Not High Frequency Tetanus Induced LTP at CA3-CA1 Synapses Within Three Hours and Devoid of an Increase in Spine Density
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Intravascular Ketamine Increases Theta-Burst but Not High Frequency Tetanus Induced LTP at CA3-CA1 Synapses Within Three Hours and Devoid of an Increase in Spine Density

机译：血管内氯胺酮可在三小时内增加θ3-爆裂但不是破伤风引起的破伤风诱导的CA3-CA1突触的LTP并且脊柱密度没有增加

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In the past 20 years, ketamine has become a promising treatment for Major Depressive Disorder (MDD) due to its rapid and sustain antidepressant effects in patients. A single ketamine treatment causes improvement in depressive symptoms within hours and can last weeks, long after it is eliminated. Previous studies have demonstrated increased synaptic plasticity at CA3-CA1 synapses in hippocampus (HPC) 24 h post ketamine treatment suggesting increased activity-dependent hippocampal function may underlie the antidepressant effects of ketamine. If true, these changes should also occur within hours of treatment, a time when symptoms are first alleviated in patients. To determine if augmented synaptic plasticity is observed at an earlier time point, we measured theta-burst and high frequency tetanus induced long-term potentiation (LTP) at CA3-CA1 synapses 3 h following intravenous (IV) ketamine administration. Additionally, we measured basal hippocampal function and spine density to investigate whether connectivity was increased with ketamine treatment. We report that theta-burst but not high frequency tetanus induced LTP is significantly increased 3 h after in vivo ketamine with no changes in basal synaptic function or morphology. Our finding supports increased activity-dependent hippocampal function underlying the antidepressant effects of ketamine as it occurs at a time point that correlates with initial improvements of depressive symptoms in patients.
机译：在过去的20年中，氯胺酮因其对患者的快速且持续的抗抑郁作用，已成为治疗重度抑郁症（MDD）的有前途的疗法。单一的氯胺酮治疗可在数小时内改善抑郁症状，并且在消除后很长时间可以持续数周。先前的研究表明，氯胺酮治疗后24小时，海马（HPC）CA3-CA1突触的突触可塑性增强，提示活动依赖性海马功能增强可能是氯胺酮抗抑郁作用的基础。如果为真，则这些变化也应在治疗后数小时内发生，这是患者首次缓解症状的时间。为了确定在较早的时间点是否观察到突触可塑性增强，我们在静脉内（IV）氯胺酮给药3小时后，测量了CA3-CA1突触的θ-爆发和高频破伤风诱发的长期增强（LTP）。此外，我们测量了基底海马功能和脊柱密度，以研究氯胺酮治疗是否增加了连通性。我们报告说，体内氯胺酮后3小时，theta爆发但不是由破伤风引起的高频LTP显着增加，而基础突触功能或形态没有变化。我们的发现支持氯胺酮抗抑郁作用的活动依赖性海马功能增强，因为氯胺酮的出现时间与患者抑郁症状的初步改善相关。

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