LaLumiere Ryan T, Pizano Emmanuel, McGaugh James L
Center for the Neurobiology of Learning and Memory, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-3800, USA.
Neurobiol Learn Mem. 2004 Jan;81(1):60-6. doi: 10.1016/s1074-7427(03)00089-3.
Previous evidence has suggested that N-methyl-D-aspartate receptors (NMDARs) in the basolateral amygdala (BLA) are critically involved in the acquisition of aversively based learning tasks. However, the role of NMDARs in the BLA in the consolidation of memory of aversive training has not been well elucidated. In the present study, the NMDAR antagonist AP-5 (1 or 3 microg) was infused into the BLA of male Sprague-Dawley rats immediately before, immediately after, or 6h after training on an inhibitory avoidance task with either a high footshock (HFS; only high dose of AP-5 given) or a low footshock (LFS; both doses of AP-5 given). The 48 h retention of animals given AP-5 (3 microg) immediately before or after HFS training was significantly impaired compared to that of vehicle-controls. In contrast, the retention of rats given AP-5 (3 microg) immediately after LFS training was significantly enhanced compared to that of vehicle-controls. AP-5 (3 microg) infusions administered 6h after training with either an HFS or LFS did not affect retention. These findings suggest that the NMDARs in the BLA are involved in both the acquisition and consolidation of aversive memory. In addition, the AP-5-induced enhancement of memory obtained with LFS training suggests that NMDARs in the BLA are involved in other mechanisms influencing synaptic transmission, in addition to their well-established role in neuroplasticity.
先前的证据表明,基底外侧杏仁核(BLA)中的N-甲基-D-天冬氨酸受体(NMDARs)在基于厌恶的学习任务的获得过程中起关键作用。然而,BLA中NMDARs在厌恶训练记忆巩固中的作用尚未得到充分阐明。在本研究中,在雄性Sprague-Dawley大鼠进行高足底电击(HFS;仅给予高剂量AP-5)或低足底电击(LFS;给予两种剂量的AP-5)抑制性回避任务训练前、训练后立即或训练后6小时,将NMDAR拮抗剂AP-5(1或3微克)注入其BLA。与给予赋形剂对照的动物相比,在HFS训练前或训练后立即给予AP-5(3微克)的动物在48小时的记忆保持显著受损。相反,与给予赋形剂对照的大鼠相比,在LFS训练后立即给予AP-5(3微克)的大鼠的记忆保持显著增强。在HFS或LFS训练后6小时给予AP-5(3微克)不影响记忆保持。这些发现表明,BLA中的NMDARs参与厌恶记忆的获得和巩固。此外,AP-5诱导的LFS训练记忆增强表明,BLA中的NMDARs除了在神经可塑性中已确立的作用外,还参与影响突触传递的其他机制。