Second-order fear conditioning prevented by blocking NMDA receptors in amygdala

摘要: Antagonists of NMDA (N-methyl-D-aspartate)-type glutamate receptors disrupt several forms learning1,2,3,4,5,6,7,8. Although this might indicate that NMDA-receptor-mediated processes are critical for synaptic plasticity, there may be other mechanisms by which NMDA-receptor antagonism could interfere with learning1,9,10,11,12. For instance, fear conditioning would blocked microinfusion the antagonist AP5 (D,L-2-amino-5-phosphonovalerate) into basolateral amygdala6,13,14 if inhibited routine transmission, thereby reducing ability stimuli to activate amygdala neurons15,16. In second-order conditioning17,18, reinforcer is a fear-eliciting conditioned stimulus rather than an unconditioned stimulus. Expression amygdala-dependent19,20 and so provides behavioural assessment neurons in presence AP5. We report here intra-amygdala actually enhances expression reinforcement signal conditioning. Nevertheless, acquisition completely blocked. Our findings strongly support view critically involved plasticity.