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首页> 外文期刊>Life sciences >Lack of interaction between NMDA and cholecystokinin-2 receptor-mediated neurotransmission in the dorsolateral periaqueductal gray in the regulation of rat defensive behaviors
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Lack of interaction between NMDA and cholecystokinin-2 receptor-mediated neurotransmission in the dorsolateral periaqueductal gray in the regulation of rat defensive behaviors

机译：NMDA和胆囊收缩素2受体介导的神经传导在背外侧导水管周围灰色区域缺乏相互作用，从而调节大鼠的防御行为

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Several neurotransmitters, including GABA, serotonin, glutamate, and cholecystokinin, modulate defensive behaviors in the dorsolateral periaqueductal gray (dIPAG). Although both glutamate and cholecystokinin have been shown to facilitate these behaviors, a possible interaction between them remains to be examined. The present study investigates whether activation or antagonism of N-methyl-D-aspartic acid (NMDA) glutamate and cholecystokinin 2 (CCK2) receptors located in the dlPAG would interact in animals tested in the elevated T-maze. The effect of the NMDA (50 pmol) was evaluated in rats pretreated with the CCK2 receptor antagonist LY225910 (0.05 nmol). In addition, the effect of the CCK2 receptor agonist CCK-4 (0.08 nmol) was evaluated in rats pretreated with the NNMA receptor antagonist AP-7 (1.0 nmol). Intra-dlPAG injection of NMDA increased risk assessment and inhibitory avoidance behaviors. This NNMA anxiogenic-like effect was unaltered by the pretreatment with LY225910. Similarly, the shortening of escape latencies induced by CCK-4 was unaffected by AP-7. No drug changed the general exploratory activity as assessed in the open-field. These results, showing that the activation of dIPAG NNMA or CCK2 receptors facilitate anxiety- and fear-related behaviors, further implicate glutamate and cholecystokinin-mediated neurotransmission in this midbrain area on modulation of defensive behaviors. However, the regulatory action of these two excitatory neurotransmitters seems to be exerted through independent mechanisms. (c) 2006 Elsevier Inc. All rights reserved.
机译：几种神经递质，包括GABA，5-羟色胺，谷氨酸和胆囊收缩素，可调节背外侧导水管周围灰色（dIPAG）的防御行为。尽管谷氨酸和胆囊收缩素均已显示出促进这些行为的作用，但它们之间可能的相互作用仍有待研究。本研究调查了位于dlPAG中的N-甲基-D-天冬氨酸（NMDA）谷氨酸和胆囊收缩素2（CCK2）受体的激活或拮抗是否会在升高的T-迷宫中测试的动物中发生相互作用。在用CCK2受体拮抗剂LY225910（0.05 nmol）预处理的大鼠中评估了NMDA（50 pmol）的作用。另外，在用NNMA受体拮抗剂AP-7（1.0nmol）预处理的大鼠中评估了CCK2受体激动剂CCK-4（0.08nmol）的作用。 dlPAG内注射NMDA可增加风险评估和抑制回避行为。 LY225910的预处理不会改变这种类似NNMA的抗焦虑作用。同样，AP-7不会影响CCK-4引起的逃逸潜伏期的缩短。在野外评估中，没有药物改变总体探索活性。这些结果表明，dIPAG NNMA或CCK2受体的激活促进了与焦虑和恐惧相关的行为，进一步暗示了谷氨酸和胆囊收缩素介导的神经传递在该中脑区域对防御行为的调节。但是，这两种兴奋性神经递质的调节作用似乎是通过独立的机制发挥的。 （c）2006 Elsevier Inc.保留所有权利。

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