Shors T J, Mathew P R
Department of Psychology and Center for Neuroscience, Rutgers University, Piscataway, New Jersey 08903, USA.
Learn Mem. 1998 Jul-Aug;5(3):220-30.
Exposure to an acute stressful event facilitates classical eye-blink conditioning in the male rat. The facilitation persists for days after the stressor and its induction is prevented by antagonism of the N-methyl-D-aspartate (NMDA) type of glutamate receptor. To determine whether NMDA receptor antagonists prevent the facilitated conditioning by activity in the amygdala, a competitive antagonist, AP5, was injected bilaterally into the lateral/basolateral versus central nuclei of the amygdala. Local injection of D,L-2-amino-5-phosphonovaleric acid (AP5) into the lateral/basolateral nucleus before stressor exposure prevented the facilitated learning 24 hr later, whereas antagonism in the central nucleus before stressor exposure did not. To determine when the necessary activation occurs, AP5 was injected into the lateral/basolateral nucleus before versus after exposure to the acute stressful event. Blockade of NMDA receptors before but not after stressor exposure prevented the facilitated acquisition of the conditioning in response to stress. These results suggest that exposure to a stressful event transiently activates NMDA receptors in basolateral/lateral nuclei of the amygdala and thereby induces a persistent enhancement of associative learning.
暴露于急性应激事件会促进雄性大鼠的经典眨眼条件反射。这种促进作用在应激源出现后的数天内持续存在，并且通过拮抗N-甲基-D-天冬氨酸（NMDA）型谷氨酸受体可阻止其诱导。为了确定NMDA受体拮抗剂是否通过杏仁核中的活动来阻止这种促进的条件反射，将竞争性拮抗剂AP5双侧注射到杏仁核的外侧/基底外侧核与中央核中。在暴露于应激源之前，将D,L-2-氨基-5-磷酸戊酸（AP5）局部注射到外侧/基底外侧核中可在24小时后阻止促进的学习，而在暴露于应激源之前对中央核进行拮抗则没有这种效果。为了确定必要的激活何时发生，在暴露于急性应激事件之前和之后将AP5注射到外侧/基底外侧核中。在应激源暴露之前而非之后阻断NMDA受体可阻止对应激的条件反射的促进获得。这些结果表明，暴露于应激事件会短暂激活杏仁核基底外侧/外侧核中的NMDA受体，从而诱导联想学习的持续增强。
