Department of Psychology, Washington State University, Pullman, WA 99164-4820, USA.
Department of Psychology, Dickinson State University, Dickinson, ND 58601, USA.
Brain Sci. 2012 Aug 20;2(3):298-318. doi: 10.3390/brainsci2030298.
The use of methamphetamine (MA) is increasing in the U.S. and elsewhere around the world. MA's capacity to cause addiction significantly exceeds other psychostimulant drugs, and its use negatively impacts learning and memory. Recently, attempts have been made to interfere with the presumed mechanism(s) underlying the establishment of drug-induced memory consolidation. The majority of these studies have employed matrix metalloproteinase (MMP) inhibitors to disrupt MMP-induced extracellular matrix molecule dependent synaptic reconfiguration, or GABA receptor agonists. The present investigation utilized an angiotensin IV (AngIV) analogue, Divalinal-AngIV (divalinal), to disrupt acquisition of MA-induced dependence in rats as measured using the conditioned place preference paradigm. Results indicate that both acute and chronic intracerebroventricular infusion of divalinal prior to each daily subcutaneous injection of MA prevented acquisition. However, divalinal was unable to prevent MA-induced reinstatement after prior acquisition followed by extinction trials. These results indicate that prevention of MA dependence can be accomplished by blockade of the brain AT4 receptor subtype. On the other hand, once MA-induced memory consolidation is in place divalinal appears to be ineffective. Mechanistic studies indicated that divalinal is a potent inhibitor of the hepatocyte growth factor (HGF)/c-Met receptor system, and thus it appears that a functional HGF/c-Met system is required for the acquisition of MA-mediated conditioned place preference.
在美国和世界其他地方,甲基苯丙胺(MA)的使用正在增加。MA 引起成瘾的能力明显超过其他精神兴奋剂药物,其使用会对学习和记忆产生负面影响。最近,人们试图干扰药物引起的记忆巩固的假定机制。这些研究大多使用基质金属蛋白酶(MMP)抑制剂来破坏 MMP 诱导的细胞外基质分子依赖性突触重排,或 GABA 受体激动剂。本研究利用血管紧张素 IV(AngIV)类似物,二缬氨酰基-AngIV(二缬氨酰基),通过条件性位置偏好范式来破坏大鼠对 MA 诱导的依赖性的获得。结果表明,急性和慢性脑室内输注二缬氨酰基在每日皮下注射 MA 之前,可以预防获得。然而,二缬氨酰基在获得后再进行消退试验后,无法防止 MA 诱导的复吸。这些结果表明,通过阻断大脑 AT4 受体亚型可以预防 MA 依赖性。另一方面,一旦 MA 诱导的记忆巩固完成,二缬氨酰基似乎就无效了。机制研究表明,二缬氨酰基是肝细胞生长因子(HGF)/c-Met 受体系统的强效抑制剂,因此,似乎需要功能性的 HGF/c-Met 系统来获得 MA 介导的条件性位置偏好。