Dietrich W D, Alonso O, Busto R, Ginsberg M D
Department of Neurology, University of Miami School of Medicine, Florida, USA.
J Neurotrauma. 1994 Dec;11(6):629-40. doi: 10.1089/neu.1994.11.629.
The effects of fluid percussion brain injury on the basal metabolic state and responsiveness of a somatosensory circuit to physiologic activation were investigated with [14C]2-deoxyglucose autoradiography. Under controlled physiologic conditions and normothermic brain temperature (37 degrees C), rats were injured with a moderate fluid percussion pulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain injury (TBI), unilateral vibrissae stimulation was carried out, resulting in the metabolic activation of the whisker-barrel circuit. In sham-operated control animals, whisker stimulation resulted in the metabolic activation of the ipsilateral trigeminal medullary complex (177% of control), contralateral ventrobasal thalamus (143% control), and primary somatosensory cortex (153% control). At 4 h after injury, local cerebral metabolic rates of glucose (ICMRglu) were significantly depressed throughout the traumatized hemisphere. Although depressed ICMRglu was most pronounced in cortical regions adjacent to the evolving contusion (53% of control), significant decreases were also seen in more remote areas, including the frontal cortex (75% of control), hippocampus (79% control), and lateral thalamus (68% of control). At 24 h following TBI, ICMRglu remained significantly reduced at the impact site, within the ipsilateral somatosensory cortex and lateral thalamus. Stimulus-evoked increases in ICMRglu were depressed within all three relay stations of the vibrissae-barrel-field circuit at 4 and 24 h after TBI. These results demonstrate both focal and diffuse metabolic depression after moderate TBI. Although the most severe and longer lasting metabolic consequences occurred in cortical and thalamic regions destined to exhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. The inability to activate the somatosensory circuit metabolically indicates that circuit dysfunction is an acute consequence of TBI. Widespread circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.
采用[14C]2-脱氧葡萄糖放射自显影术，研究了液压冲击性脑损伤对基础代谢状态以及体感回路对生理激活反应性的影响。在受控生理条件和正常脑温（37℃）下，用1.7至2.1个大气压的中等强度液压冲击脉冲对大鼠造成损伤。在创伤性脑损伤（TBI）后4小时或24小时，进行单侧触须刺激，从而导致触须-桶状回路的代谢激活。在假手术对照动物中，触须刺激导致同侧三叉神经髓质复合体代谢激活（为对照的177%）、对侧腹后基底丘脑代谢激活（为对照的143%）以及初级体感皮层代谢激活（为对照的153%）。损伤后4小时，整个受创伤半球的局部脑葡萄糖代谢率（ICMRglu）显著降低。虽然降低的ICMRglu在临近正在形成的挫伤的皮质区域最为明显（为对照的53%），但在包括额叶皮质（为对照的75%）、海马体（为对照的79%）和外侧丘脑（为对照的68%）等更远的区域也可见显著降低。TBI后24小时，在撞击部位、同侧体感皮层和外侧丘脑内，ICMRglu仍显著降低。在TBI后4小时和24小时，触须-桶状场回路的所有三个中继站中，刺激诱发的ICMRglu增加均受到抑制。这些结果表明中度TBI后存在局灶性和弥漫性代谢抑制。虽然最严重且持续时间更长的代谢后果发生在注定会出现组织病理学损伤的皮质和丘脑区域，但在未受伤区域也可见到较轻的异常，在创伤后早期最为明显。无法在代谢上激活体感回路表明回路功能障碍是TBI的急性后果。预计广泛的回路或突触功能障碍会参与TBI的功能和行为后果。
