Troncoso Julieta, Maldonado Héctor
Laboratorio de Neurobiología de la Memoria, Facultad de Ciencias Exactas y Naturales, Departamento Biologia, Universidad de Buenos Aires, Buenos Aires, Argentina.
Pharmacol Biochem Behav. 2002 May;72(1-2):251-65. doi: 10.1016/s0091-3057(01)00779-1.
A visual danger stimulus (VDS) elicits an escape response in the crab Chasmagnathus that declines after a few iterative presentations. Long-lasting retention of such decrement, termed context-signal memory (CSM), is mediated by an association between danger stimulus and environmental cues, cycloheximide sensitive, correlated with PKA activity and NFkappa-B activation, positively modulated by angiotensins, and selectively regulated by a muscarinic-cholinergic mechanism. The present research was aimed at studying the possible involvement of NMDA-like receptors in CSM, given the role attributed to these receptors in vertebrate memory and their occurrence in invertebrates including crustaceans. Vertebrate antagonists (+/-)-2-amino-5-phosphonopentanoic acid (AP5) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) were used. Memory retention impairment was shown with MK-801 10(-3) M (1 microg/g) injected immediately before training or after training, or delayed 1 or 4 h, but not 6 h, posttraining. An AP5 10(-3) M dose (0.6 microg/g) impairs retention when given before but not after training. Neither antagonist produced retrieval deficit. A memory process similar to CSM but nonassociative in nature and induced by massed training (termed signal memory, SM), proved entirely insensitive to AP5 or MK-801, confirming the view that distinct mechanisms subserve these different types of memory in the crab.
视觉危险刺激(VDS)会引发招潮蟹的逃避反应,该反应在经过几次重复呈现后会减弱。这种减弱的长期保持,即所谓的情境信号记忆(CSM),是由危险刺激与环境线索之间的关联介导的,对放线菌酮敏感,与蛋白激酶A活性和核因子κB激活相关,受血管紧张素正向调节,并由毒蕈碱胆碱能机制选择性调节。鉴于这些受体在脊椎动物记忆中的作用以及它们在包括甲壳类动物在内的无脊椎动物中的存在,本研究旨在探讨NMDA样受体在CSM中可能的参与情况。使用了脊椎动物拮抗剂(±)-2-氨基-5-磷酸戊酸(AP5)和(+)-5-甲基-10,11-二氢-5H-二苯并[a,d]环庚烯-5,10-亚胺(MK-801)。在训练前、训练后立即注射或训练后延迟1或4小时(但不是6小时)注射10-3 M(1微克/克)的MK-801,会导致记忆保持受损。在训练前给予10-3 M剂量(0.6微克/克)的AP5会损害记忆保持,但在训练后给予则不会。两种拮抗剂均未产生检索缺陷。一种类似于CSM但本质上是非联想性的、由集中训练诱导的记忆过程(称为信号记忆,SM),被证明对AP5或MK-801完全不敏感,这证实了不同机制服务于螃蟹中这些不同类型记忆的观点。