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首页> 外文期刊>BMC Neuroscience >Effects of the group I metabotropic glutamate receptor agonist, DHPG, and injection stress on striatal cell signaling in food-restricted and ad libitum fed rats
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Effects of the group I metabotropic glutamate receptor agonist, DHPG, and injection stress on striatal cell signaling in food-restricted and ad libitum fed rats

机译：Ⅰ类代谢型谷氨酸受体激动剂DHPG和注射应激对禁食和随意喂养大鼠纹状体细胞信号的影响

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Background Chronic food restriction augments the rewarding effect of centrally administered psychostimulant drugs and this effect may involve a previously documented upregulation of D-1 dopamine receptor-mediated MAP kinase signaling in nucleus accumbens (NAc) and caudate-putamen (CPu). Psychostimulants are known to induce striatal glutamate release, and group I metabotropic glutamate receptors (mGluR) have been implicated in the cellular and behavioral responses to amphetamine. The purpose of the present study was to evaluate whether chronic food restriction increases striatal MAP kinase signaling in response to the group I mGluR agonist, DHPG. Results Western immunoblotting was used to demonstrate that intracerebroventricular (i.c.v.) injection of DHPG (500 nmol) produces greater activation of ERK1/2 and CREB in CPu and NAc of food-restricted as compared to ad libitum fed rats. Fos-immunostaining induced by DHPG was also stronger in CPu and NAc core of food-restricted relative to ad libitum fed rats. However, i.c.v. injection of saline-vehicle produced greater activation of ERK1/2 and CREB in CPu and NAc of food-restricted relative to ad libitum fed rats, and this difference was not seen when subjects received no i.c.v. injection prior to sacrifice. In addition, although DHPG activated Akt, there was no difference in Akt activation between feeding groups. To probe whether the augmented ERK1/2 and CREB activation in vehicle-injected food-restricted rats are mediated by one or more GluR types, effects of an NMDA antagonist (MK-801, 100 nmol), AMPA antagonist (DNQX, 10 nmol), and group I mGluR antagonist (AIDA, 100 nmol) were compared to saline-vehicle. Antagonist injections did not diminish activation of ERK1/2 or CREB. Conclusions These results indicate that a group I mGluR agonist induces phosphorylation of Akt, ERK1/2 and CREB in both CPu and NAc. However, group I mGluR-mediated signaling may not be upregulated in food-restricted rats. Rather, a physiological response to "i.c.v. injection stress" is augmented by food restriction and appears to summate with effects of the group I mGluR agonist in activating ERK1/2 and CREB. While the augmented cellular response of food-restricted rats to i.c.v. injection treatment represents additional evidence of enhanced CNS responsiveness in these subjects, the functional significance and underlying mechanism(s) of this effect remain to be elucidated.
机译：背景长期食物限制会增强集中使用的精神刺激药的奖励作用，这种作用可能涉及先前记载的伏伏核（NAc）和尾状豆核（CPu）中D-1多巴胺受体介导的MAP激酶信号上调。已知精神兴奋剂可诱导纹状体谷氨酸释放，并且I组代谢型谷氨酸受体（mGluR）与对苯丙胺的细胞和行为反应有关。本研究的目的是评估慢性食物限制是否会响应I组mGluR激动剂DHPG，增加纹状体MAP激酶信号传导。结果免疫印迹法被用来证明脑室内（i.c.v.）注射DHPG（500 nmol）与自由进食大鼠相比，在食物受限的CPu和NAc中产生更大的ERK1 / 2和CREB活化。 DHPG诱导的Fos免疫染色在食物受限的CPu和NAc核心中相对于随意喂养的大鼠更强。但是，相对于随意喂食的大鼠，注射盐水的车辆在受食物限制的CPu和NAc中产生了更大的ERK1 / 2和CREB激活，并且当受试者未接受腹腔静脉注射时，未观察到这种差异。牺牲前注射。此外，尽管DHPG激活了Akt，但喂养组之间的Akt激活没有差异。为了探讨是否通过一种或多种GluR类型介导了经媒介物限制饮食的大鼠中ERK1 / 2和CREB激活的增强，NMDA拮抗剂（MK-801，100 nmol），AMPA拮抗剂（DNQX，10 nmol）的作用，并将I组mGluR拮抗剂（AIDA，100 nmol）与盐水车进行比较。拮抗剂注射并没有减少ERK1 / 2或CREB的激活。结论这些结果表明，I类mGluR激动剂在CPu和NAc中诱导Akt，ERK1 / 2和CREB的磷酸化。但是，在食物限制的大鼠中，I类mGluR介导的信号传导可能不会被上调。相反，对“ i.c.v.注射应力”的生理反应通过食物限制而增强，并且似乎与I类mGluR激动剂在激活ERK1 / 2和CREB中的作用相加。禁食大鼠对i.c.v的细胞反应增强。注射治疗代表了这些受试者中枢神经系统反应增强的其他证据，这种作用的功能重要性和潜在机制尚待阐明。

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