Excitatory amino acid receptor activation in the raphe pallidus area mediates prostaglandin-evoked thermogenesis
Excitatory amino acid receptor activation in the raphe pallidus area mediates prostaglandin-evoked thermogenesis
复制标题
DOI：
10.1016/s0306-4522(03)00527-x
复制
发表时间：
2003-01-01
期刊：
影响因子：
3.3
通讯作者：
Morrison, SF
中科院分区：
文献类型：
--
作者：
Madden, CJ;Morrison, SF
为探讨中缝苍白区（RPa）内兴奋性氨基酸神经传递在产热反应和心血管反应中的作用，在氯醛糖麻醉、通气的大鼠RPa内微量注射兴奋性氨基酸（EAA）受体激动剂后，记录交感神经对棕色脂肪组织（BAT）的活动、BAT温度、呼出CO2、动脉压和心率的变化。为了确定RPa内的EAA神经传递是否是由RPa的去抑制或由在内侧视前区内起作用的前列腺素E-2诱发的反应所必需的，在这些治疗期间在RPa内的EAA受体阻断之前和之后测量BAT交感神经活性、BAT温度、呼出的CO2、动脉压和心率。微量注射EAA受体激动剂到RPa中导致所有测量变量的显著增加;这些增加通过预先微量注射各自的EAA受体拮抗剂到RPa中而减弱。视前内侧区微量注射前列腺素E-2或RPa区微量注射荷包牡丹碱，BAT交感神经活动均显著增加（+约190%和+约235%的静息水平），BAT温度（约1.8 ℃和约2 ℃），在呼出的CO2中1%和约1.1%）和心率（约97次/分钟（bpm）和约100 bpm）。通过微量注射犬尿酸盐阻断RPa内的离子型EAA受体完全逆转了前列腺素E-2或荷包牡丹碱诱发的所有测量变量的增加。阻断N-甲基-D-天冬氨酸（NMDA）受体或非NMDA受体单独导致前列腺素E-2引起的所有测量变量的影响显着衰减。这些数据表明，激活EAA输入到RPa是必要的BAT产热和心血管的影响，导致前列腺素E-2的行动内的内侧视前区或从局部神经元的RPa的去抑制。(C)2003年IBRO。由爱思唯尔有限公司出版。保留所有权利。
To investigate the role of excitatory amino acid neurotransmission within the rostral raphe pallidus area (RPa) in thermogenic and cardiovascular responses, changes in sympathetic nerve activity to brown adipose tissue (BAT), BAT temperature, expired CO2, arterial pressure, and heart rate were recorded after microinjection of excitatory amino acid (EAA) receptor agonists into the RPa in urethan-chloralose-anesthetized, ventilated rats. To determine whether EAA neurotransmission within the RPa is necessary for the responses evoked by disinhibition of the RPa or by prostaglandin E-2 acting within the medial preoptic area, BAT sympathetic nerve activity, BAT temperature, expired CO2, arterial pressure, and heart rate were measured during these treatments both before and after blockade of EAA receptors within the RPa. Microinjection of EAA receptor agonists into the RPa resulted in significant increases in all measured variables; these increases were attenuated by prior microinjection of the respective EAA receptor antagonists into the RPa. Microinjection of prostaglandin E-2 into the medial preoptic area or microinjection of bicuculline into the RPa resulted in respective significant increases in BAT sympathetic nerve activity (+approximately 190% and +approximately 235% of resting levels), in BAT temperature (approximately 1.8 degreesC and approximately 2 degreesC), in expired CO2 (approximately 1.1% and approximately 1.1%), and in heart rate (approximately 97 beats per minute (bpm) and approximately 100 bpm). Blockade of ionotropic EAA receptors within the RPa by microinjection of kynurenate completely reversed the prostaglandin E-2 or bicuculline-evoked increases in all of the measured variables. Blockade of either N-methyl-D-aspartate (NMDA) receptors or non-NMDA receptors alone resulted in marked attenuations of the prostaglandin E-2-evoked effects on all of the measured variables. These data demonstrate that activation of an EAA input to the RPa is necessary for the BAT thermogenic and the cardiovascular effects resulting from the actions of prostaglandin E-2 within the medial preoptic area or from the disinhibition of local neurons in the RPa. (C) 2003 IBRO. Published by Elsevier Ltd. All rights reserved.