Evidence for a kynurenate-insensitive glutamate receptor in nucleus tractus solitarii.
Evidence for a kynurenate-insensitive glutamate receptor in nucleus tractus solitarii.
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孤束核中存在对犬尿酸盐不敏感的谷氨酸受体的证据。
DOI：
10.1152/ajpheart.1992.262.5.h1611
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Gordon,FJ
中科院分区：
文献类型：
--
作者：
Pawloski-Dahm,C;Gordon,FJ
先前的研究表明，用犬尿酸钠（Kyn）对孤束核（NTS）中的离子型兴奋性氨基酸（EAA）受体进行药理学阻断，可以消除压力感受性反射，但未能影响通过微量注射L-谷氨酸（Glu）诱发的心血管反应。进入NTS。这些观察结果提出了疑问，是否谷氨酸是一种神经递质的压力感受器信息的NTS，因为外源性管理的谷氨酸的药理作用是不相同的神经递质释放的NTS与压力感受器激活。对这些结果的一个可能的解释是，外源性施用的Glu可能作用于不被Kyn阻断的受体，并且在NTS压力感受器反射通路中不能接近突触释放的Glu。本研究的目的是确定Kyn不敏感的Glu受体是否存在于NTS中。这种Kyn不敏感受体的一个候选者是由反式-DL-1-氨基-1，3-环戊烷-二羧酸（ACPD）选择性激活的代谢型EAA受体。将ACPD微量注射到麻醉大鼠的NTS中产生剂量相关的降压反应，Kyn或用假定的ACPD受体拮抗剂L-2-氨基-3-膦酰基丙酸酯（L-AP-3）预处理不降低该降压反应。类似地，Glu产生的降压反应也不受Kyn或L-AP-3的影响。这些数据表明NTS中存在Kyn不敏感的Glu受体。此外，他们认为，Kyn未能减少由Glu注射到NTS引起的心血管反应，这可以通过Glu对Kyn不敏感的ACPD受体的作用来解释。（250字处删节）
Previous studies have shown that pharmacological blockade of ionotropic excitatory amino acid (EAA) receptors in the nucleus tractus solitarii (NTS) with kynurenate (Kyn) abolishes baroreceptor reflexes but fails to affect cardiovascular responses evoked by microinjections of L-glutamate (Glu) into the NTS. These observations have raised doubts as to whether Glu is a neurotransmitter of baroreceptor information in the NTS because the pharmacological actions of exogenously administered Glu are not identical to those of the neurotransmitter released in the NTS coincident with baroreceptor activation. One possible explanation for these results is that exogenously administered Glu might act at receptors that are not blocked by Kyn and are not accessible to synaptically released Glu in the NTS baroreflex pathway. The purpose of this study was to determine if Kyn-insensitive Glu receptors are present in the NTS. One candidate for this Kyn-insensitive receptor is the metabotropic EAA receptor that is selectively activated by trans-DL-1-amino-1,3-cyclopentane-dicarboxylic acid (ACPD). Microinjections of ACPD into the NTS of anesthetized rats produced dose-related depressor responses that were not reduced by Kyn or by pretreatment with the putative ACPD receptor antagonist L-2-amino-3-phosphonopropionate (L-AP-3). Similarly, depressor responses produced by Glu also were not affected by Kyn or by L-AP-3. These data demonstrate the presence of a Kyn-insensitive Glu receptor in the NTS. Moreover, they suggest that the failure of Kyn to reduce cardiovascular responses evoked by Glu injections into the NTS can be explained by an action of Glu at Kyn-insensitive ACPD receptors.(ABSTRACT TRUNCATED AT 250 WORDS)