Acute lipopolysaccharide (LPS) administration induces innate inflammatory signalling and produces sickness reaction characterized by reduced drinking, eating and reduced locomotor exploration, as well as emotional changes indicating increased helplessness/despair. LPS administration has been used to model behavioral and emotional responses to inflammatory reactions. Our aim was to find out whether the lack of metabotropic glutamate receptor 3 (mGluR3) in the knockout (KO) mice affects behavioral effects of LPS in vivo, as mGluR3 may have a role in inflammatory signalling. After LPS (1 mg/kg, i.p.) administration, we compared wild-type (WT) and mGluR3-KO mice for differences in gross appearance and locomotion at 3- and 6-h time points, anxiety-like behavior in the light-dark test at 24-h, depression-like behavior in the tail-suspension test at 25-h, and in the forced-swim test at 48-h time points. Body weight and water consumption were monitored. Based on behavioral scorings at the 3-h and 6-h time points, the mGluR3-KO mice reacted to LPS in a similar way as the WT mice. LPS-induced reductions in the body weight or water consumption did not differ between genotypes. Interestingly, LPS-induced reductions in the body temperature were significantly enhanced in male and female mGluR3-KO mice at 6-h and 3-h time points, respectively. In the light-dark anxiety-test the saline-treated mGluR3-KOs showed increased anxiolytic-like behaviors compared to the saline-treated WT mice. LPS treatment significantly reduced the KO entries to the light compartment to the same level as WT mice given saline. Total locomotion was significantly reduced in both genotypes by LPS. In the despair models, no genotype difference was observed after saline or LPS, neither had LPS treatment any significant effect on immobility. Although changes in glutamatergic neurotransmission may partly mediate effects of systemic LPS administration, mGluR3 appears not to be crucial in behavioral responses to acute activation of innate immune system.

急性脂多糖（LPS）给药会诱发先天性炎症信号并产生疾病反应，其特征是饮酒，进食和运动探索减少，以及情绪变化表明无助/绝望增加。LPS给药已被用于模拟对炎症反应的行为和情绪反应。我们的目的是找出基因敲除（KO）小鼠中代谢型谷氨酸受体3（mGluR3）的缺乏是否会影响LPS在体内的行为效应，因为mGluR3可能在炎症信号传导中起作用。给予LPS（1 mg / kg，ip）后，我们比较了野生型（WT）和mGluR3-KO小鼠在3小时和6小时时间的总体外观和运动差异，在光照下的焦虑样行为在24小时内进行黑暗测试，在25小时后进行尾部悬吊测试，表现出类似抑郁的表现，并在48小时的时间点进行强制游泳测试。监测体重和水消耗。根据在3小时和6小时时间点的行为评分，mGluR3-KO小鼠对LPS的反应与WT小鼠相似。LPS引起的体重或水消耗的减少在基因型之间没有差异。有趣的是，LPS诱导的体温下降在雄性和雌性mGluR3-KO小鼠中分别在6小时和3小时的时间点显着增强。在光暗焦虑测试中，与生理盐水处理的WT小鼠相比，生理盐水处理的mGluR3-KOs表现出更高的抗焦虑样行为。LPS处理显着降低了进入轻型隔室的KO进入水平，使其与给予盐水的WT小鼠相同。LPS使两种基因型的总运动明显降低。在绝望模型中 盐水或LPS后未观察到基因型差异，LPS处理均未对固定性产生任何显着影响。尽管谷氨酸能神经传递的变化可能部分介导了全身性LPS给药的作用，但mGluR3在对先天免疫系统急性激活的行为反应中似乎并不关键。