Barsegyan Areg, Atsak Piray, Hornberger Wilfried B, Jacobson Peer B, van Gaalen Marcel M, Roozendaal Benno
1] Department of Cognitive Neuroscience, Radboud University Medical Centre, Nijmegen, The Netherlands [2] Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, Nijmegen, The Netherlands.
Neuroscience Research, AbbVie Deutschland GmbH & Co KG, Ludwigshafen, Germany.
Neuropsychopharmacology. 2015 Jul;40(8):1979-89. doi: 10.1038/npp.2015.48. Epub 2015 Feb 11.
Stress-induced activation of the hypothalamo-pituitary-adrenocortical (HPA) axis and high circulating glucocorticoid levels are well known to impair the retrieval of memory. Vasopressin can activate the HPA axis by stimulating vasopressin 1b (V1b) receptors located on the pituitary. In the present study, we investigated the effect of A-988315, a selective and highly potent non-peptidergic V1b-receptor antagonist with good pharmacokinetic properties, in blocking stress effects on HPA-axis activity and memory retrieval. To study cognitive performance, male Sprague-Dawley rats were trained on an object-discrimination task during which they could freely explore two identical objects. Memory for the objects and their location was tested 24 h later. A-988315 (20 or 60 mg/kg) or water was administered orally 90 min before retention testing, followed 60 min later by stress of footshock exposure. A-988315 dose-dependently dampened stress-induced increases in corticosterone plasma levels, but did not significantly alter HPA-axis activity of non-stressed control rats. Most importantly, A-988315 administration prevented stress-induced impairment of memory retrieval on both the object-recognition and the object-location tasks. A-988315 did not alter the retention of non-stressed rats and did not influence the total time spent exploring the objects or experimental context in either stressed or non-stressed rats. Thus, these findings indicate that direct antagonism of V1b receptors is an effective treatment to block stress-induced activation of the HPA axis and the consequent impairment of retrieval of different aspects of recognition memory.
应激诱导的下丘脑 - 垂体 - 肾上腺皮质(HPA)轴激活和高循环糖皮质激素水平会损害记忆提取,这是众所周知的。血管加压素可通过刺激位于垂体上的血管加压素1b(V1b)受体来激活HPA轴。在本研究中,我们研究了A - 988315(一种具有良好药代动力学特性的选择性且高效的非肽类V1b受体拮抗剂)在阻断应激对HPA轴活性和记忆提取的影响方面的作用。为了研究认知能力,对雄性Sprague - Dawley大鼠进行物体辨别任务训练,在此期间它们可以自由探索两个相同的物体。24小时后测试对物体及其位置的记忆。在保留测试前90分钟口服给予A - 988315(20或60mg / kg)或水,60分钟后进行足部电击应激。A - 988315剂量依赖性地抑制了应激诱导的皮质酮血浆水平升高,但未显著改变非应激对照大鼠的HPA轴活性。最重要的是,给予A - 988315可防止应激诱导的物体识别和物体定位任务中的记忆提取受损。A - 988315不会改变非应激大鼠的记忆保留,也不会影响应激或非应激大鼠探索物体或实验环境所花费的总时间。因此,这些发现表明,直接拮抗V1b受体是一种有效的治疗方法,可阻断应激诱导的HPA轴激活以及随之而来的识别记忆不同方面的提取受损。