Conceição Ellen Paula Santos da, Madden Christopher J, Morrison Shaun F
Department of Neurological Surgery, Oregon Health & Science University, Portland, Oregon
Department of Neurological Surgery, Oregon Health & Science University, Portland, Oregon.
Am J Physiol Regul Integr Comp Physiol. 2017 Jun 1;312(6):R919-R926. doi: 10.1152/ajpregu.00551.2016. Epub 2017 Mar 2.
The rostral raphe pallidus (rRPa) contains sympathetic premotor neurons controlling thermogenesis in brown adipose tissue (BAT). We sought to determine whether a tonic activation of glycine receptors (GlyR) in the rRPa contributes to the inhibitory regulation of BAT sympathetic nerve activity (SNA) and of cardiovascular parameters in anesthetized rats. Nanoinjection of the GlyR antagonist, strychnine (STR), into the rRPa of intact rats increased BAT SNA (peak: +495%), BAT temperature (T, +1.1°C), expired CO, (+0.4%), core body temperature (T, +0.2°C), mean arterial pressure (MAP, +4 mmHg), and heart rate (HR, +57 beats/min). STR into rRPa in rats with a postdorsomedial hypothalamus transection produced similar increases in BAT thermogenic and cardiovascular parameters. Glycine nanoinjection into the rRPa evoked a potent inhibition of the cooling-evoked increases in BAT SNA (nadir: -74%), T (-0.2°C), T (-0.2°C), expired CO (-0.2%), MAP (-8 mmHg), and HR (-22 beats/min) but had no effect on the increases in these variables evoked by STR nanoinjection into rRPa. Nanoinjection of GABA into the rRPa inhibited the STR-evoked BAT SNA (nadir: -86%) and reduced the expired CO (-0.4%). Blockade of glutamate receptors in rRPa reduced the STR-evoked increases in BAT SNA (nadir: -61%), T (-0.5°C), expired CO (-0.3%), MAP (-9 mmHg), and HR (-33 beats/min). We conclude that a tonically active glycinergic input to the rRPa contributes to the inhibitory regulation of the discharge of BAT sympathetic premotor neurons and of BAT thermogenesis and energy expenditure.
延髓头端中缝苍白核（rRPa）含有控制棕色脂肪组织（BAT）产热的交感运动前神经元。我们试图确定rRPa中甘氨酸受体（GlyR）的持续性激活是否有助于抑制麻醉大鼠的BAT交感神经活动（SNA）和心血管参数。向完整大鼠的rRPa中微量注射GlyR拮抗剂士的宁（STR），可增加BAT SNA（峰值：+495%）、BAT温度（T，+1.1°C）、呼出CO₂（+0.4%）、核心体温（T，+0.2°C）、平均动脉压（MAP，+4 mmHg）和心率（HR，+57次/分钟）。在背内侧下丘脑横断的大鼠中，向rRPa注射STR可使BAT产热和心血管参数产生类似的增加。向rRPa中微量注射甘氨酸可有效抑制冷却引起的BAT SNA增加（最低点：-74%）、T（-0.2°C）、T（-0.2°C）、呼出CO₂（-0.2%）、MAP（-8 mmHg）和HR（-22次/分钟），但对向rRPa中微量注射STR引起的这些变量增加没有影响。向rRPa中微量注射GABA可抑制STR引起的BAT SNA（最低点：-86%），并降低呼出CO₂（-0.4%）。阻断rRPa中的谷氨酸受体可降低STR引起的BAT SNA增加（最低点：-61%）、T（-0.5°C）、呼出CO₂（-0.3%）、MAP（-9 mmHg）和HR（-33次/分钟）。我们得出结论，rRPa中持续活跃的甘氨酸能输入有助于抑制BAT交感运动前神经元的放电以及BAT产热和能量消耗。
