Hayward Linda F
University of Florida, College of Veterinary Medicine, Department of Physiological Sciences and McKnight Brain Institute, PO 100144 Gainesville, FL 32610-1044, USA.
Brain Res. 2007 May 11;1145:117-27. doi: 10.1016/j.brainres.2007.01.140. Epub 2007 Feb 16.
Activation of the dorsal periaqueductal gray (PAG) evokes defense-like behavior including a marked increase in sympathetic drive and resetting of baroreflex function. The goal of this study was to investigate the role of the lateral parabrachial nucleus (LPBN) in mediating dorsal PAG modulation of the arterial baroreflex. Reflex responses were elicited by electrical stimulation of the aortic depressor nerve (ADN) at 5 Hz or 15 Hz in urethane anesthetized rats (n=18). Electrical stimulation of the dorsal PAG at 10 Hz did not alter baseline mean arterial pressure (MAP) but did significantly attenuate baroreflex control of heart rate (HR) evoked by low frequency ADN stimulation. Alternatively, 40 Hz dorsal PAG stimulation increased baseline MAP (43+/-3 mm Hg) and HR (33+/-3 bpm) and attenuated baroreflex control of HR at both ADN stimulation frequencies. Reflex control of MAP was generally unchanged by dorsal PAG stimulation. Bilateral inhibition of neurons in LPBN area (n=6) with muscimol (0.45 nmol per side) reduced dorsal PAG-evoked increases in MAP and HR by 50+/-4% and 95+/-4%, respectively, and significantly reduced, but did not completely eliminate dorsal PAG attenuation of the cardiac baroreflex. Bilateral blockade of glutamate receptors in the LPBN area (n=6) with kynurenic acid (1.8 nmol) had a similar effect on dorsal PAG-evoked increases in MAP, HR and cardiac baroreflex function. Reflex control of MAP was unchanged with either treatment. These findings suggest that the LPBN area is one of several brainstem regions involved in descending modulation of the cardiac baroreflex function during defensive behavior.
中脑导水管周围灰质背侧(PAG)的激活会引发类似防御的行为,包括交感神经驱动显著增加以及压力感受性反射功能的重置。本研究的目的是探究臂旁外侧核(LPBN)在介导PAG背侧对动脉压力感受性反射调节中的作用。在乌拉坦麻醉的大鼠(n = 18)中,通过以5 Hz或15 Hz的频率电刺激主动脉减压神经(ADN)来引发反射反应。以10 Hz的频率电刺激PAG背侧不会改变基线平均动脉压(MAP),但会显著减弱低频ADN刺激所诱发的心率(HR)压力感受性反射控制。另外,40 Hz的PAG背侧刺激会增加基线MAP(43±3 mmHg)和HR(33±3 bpm),并在两个ADN刺激频率下均减弱HR的压力感受性反射控制。PAG背侧刺激通常不会改变MAP的反射控制。用蝇蕈醇(每侧0.45 nmol)对LPBN区域的神经元进行双侧抑制(n = 6),分别使PAG背侧诱发的MAP和HR增加降低了50±4%和95±4%,并显著降低但并未完全消除PAG背侧对心脏压力感受性反射的减弱作用。用犬尿氨酸(1.8 nmol)对LPBN区域的谷氨酸受体进行双侧阻断(n = 6),对PAG背侧诱发的MAP、HR增加以及心脏压力感受性反射功能具有类似作用。两种处理方式下MAP的反射控制均未改变。这些发现表明,LPBN区域是在防御行为期间参与心脏压力感受性反射功能下行调制的几个脑干区域之一。