Tanaka Mutsumi, Owens Neil C, Nagashima Kei, Kanosue Kazuyuki, McAllen Robin M
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia.
J Physiol. 2006 Apr 15;572(Pt 2):569-83. doi: 10.1113/jphysiol.2005.102400. Epub 2006 Feb 16.
The nature of muscle efferent fibre activation during whole body cooling was investigated in urethane-anaesthetized rats. Multiunit efferent activity to the gastrocnemius muscle was detected when the trunk skin was cooled by a water-perfused jacket to below 36.0 +/- 0.7 degrees C. That efferent activity was not blocked by hexamethonium (50 mg kg(-1), i.v.) and was not associated with movement or electromyographic activity. Cold-induced efferent activity enhanced the discharge of afferent filaments from the isotonically stretched gastrocnemius muscle, demonstrating that it was fusimotor. Fusimotor neurons were activated by falls in trunk skin temperature, but that activity ceased when the skin was rewarmed, regardless of how low core temperature had fallen. While low core temperature alone was ineffective, a high core temperature could inhibit the fusimotor response to skin cooling. Fusimotor activation by skin cooling was often accompanied by desynchronization of the frontal electroencephalogram (EEG), but was not a simple consequence of cortical arousal, in that warming the scrotum desynchronized the EEG without activating fusimotor fibres. Inhibition of neurons in the rostral medullary raphé by microinjections of glycine (0.5 m, 120-180 nl) reduced the fusimotor response to skin cooling by 95 +/- 3%, but did not prevent the EEG response. These results are interpreted as showing a novel thermoregulatory reflex that is triggered by cold exposure. It may underlie the increased muscle tone that precedes overt shivering, and could also serve to amplify shivering. Like several other cold-defence responses, this reflex depends upon neurons in the rostral medullary raphé.
在氨基甲酸乙酯麻醉的大鼠中,研究了全身冷却过程中肌肉传出纤维激活的性质。当用灌注水的外套将大鼠躯干皮肤冷却至36.0±0.7℃以下时,检测到腓肠肌的多单位传出活动。该传出活动不受六甲铵(50mg kg⁻¹,静脉注射)的阻断,且与运动或肌电图活动无关。冷诱导的传出活动增强了等张拉伸的腓肠肌传入纤维的放电,表明其为肌梭运动纤维。肌梭运动神经元因躯干皮肤温度下降而被激活,但当皮肤复温时,该活动停止,无论核心温度下降到多低。虽然单独的低核心温度无效,但高核心温度可抑制对皮肤冷却的肌梭运动反应。皮肤冷却引起的肌梭运动激活常伴有额叶脑电图(EEG)的去同步化,但并非皮层觉醒的简单结果,因为阴囊升温使EEG去同步化而未激活肌梭运动纤维。通过微量注射甘氨酸(0.5m,120 - 180nl)抑制延髓头端中缝核的神经元,可使对皮肤冷却的肌梭运动反应降低95±3%,但不影响EEG反应。这些结果被解释为显示了一种由冷暴露触发的新型体温调节反射。它可能是明显寒战之前肌肉张力增加的基础,也可能有助于增强寒战。与其他几种冷防御反应一样,这种反射依赖于延髓头端中缝核的神经元。