Muthuswamy J, Kimura T, Ding M C, Geocadin R, Hanley D F, Thakor N V
Department of Bioengineering, PO Box 879709, College of Engineering and Applied Sciences, Arizona State University, Tempe, AZ 85287-9709, USA.
Neuroscience. 2002;115(3):917-29. doi: 10.1016/s0306-4522(02)00369-x.
The aim of this study was to test the hypothesis that under prolonged global ischemic injury, the somatosensory thalamus and the cortex would manifest differential susceptibility leading to varying degrees of thalamo-cortical dissociation. The thalamic electrical responses displayed increasing suppression with longer durations of ischemia leading to a significant thalamo-cortical electrical dissociation. The data also point to a selective vulnerability of the network oscillations involving the thalamic relay and reticular thalamic neurons. An adult rat model of asphyxial cardiac arrest involving three cohorts with 3 min (G1, n=5), 5 min (G2, n=5) and 7 min (G3, n=5) of asphyxia respectively was used. The cortical evoked response, as quantified by the peak amplitude at 20 ms in the cortical evoked potential, recovers to more than 60% of baseline in all the cases. The multi-unit responses to the somatosensory stimuli recorded from the thalamic ventral posterior lateral (VPL) nuclei consists typically of three components: (1). the ON response (<30 ms after stimulus), (2). the OFF response (period of inhibition, from 30 ms to 100 ms after stimulus) and (3). rhythmic spindles (beyond 100 ms after stimulus). Asphyxia has a significant effect on the VPL ON response at 30 min (P<0.025), 60 min (P<0.05) and 90 min (P<0.05) after asphyxia. Only animals in G3 show a significant suppression (P<0.05) of the VPL ON response when compared to the sham group at 30 min, 60 min and 90 min after asphyxia. There was no significant reduction in somatosensory cortical N20 (negative peak in the cortical response at 20 ms after stimulus) amplitude in any of the three groups with asphyxia indicating a thalamo-cortical dissociation in G3. Further, rhythmic spindle oscillations in the thalamic VPL nuclei that normally accompany the ON response recover either slowly after the recovery of ON response (in the case of G1 and G2) or do not recover at all (in the case of G3).We conclude that there is strong evidence for selective vulnerability of thalamic relay neurons and its network interactions with the inhibitory interneurons in the somatosensory pathway leading to a thalamo-cortical dissociation after prolonged durations of global ischemia.
在长时间的全脑缺血性损伤下，体感丘脑和皮层会表现出不同的易损性，从而导致不同程度的丘脑 - 皮层分离。随着缺血时间延长，丘脑电反应的抑制作用增强，导致明显的丘脑 - 皮层电分离。数据还表明，涉及丘脑中继神经元和丘脑网状神经元的网络振荡存在选择性易损性。采用成年大鼠窒息性心脏骤停模型，分为三个队列，分别进行3分钟（G1，n = 5）、5分钟（G2，n = 5）和7分钟（G3，n = 5）的窒息。皮层诱发电位中以20毫秒时的峰值幅度量化的皮层诱发反应，在所有情况下均恢复到基线的60%以上。从丘脑腹后外侧（VPL）核记录到的对体感刺激的多单位反应通常由三个成分组成：（1）. 开启反应（刺激后<30毫秒），（2）. 关闭反应（抑制期，刺激后30毫秒至100毫秒）和（3）. 节律性纺锤波（刺激后100毫秒以上）。窒息对窒息后30分钟（P<0.025）、60分钟（P<0.05）和90分钟（P<0.05）的VPL开启反应有显著影响。与假手术组相比，仅G3组动物在窒息后30分钟、60分钟和90分钟时VPL开启反应有显著抑制（P<0.05）。三个窒息组中任何一组的体感皮层N20（刺激后20毫秒时皮层反应中的负峰）幅度均无显著降低，表明G3组存在丘脑 - 皮层分离。此外，通常伴随开启反应的丘脑VPL核中的节律性纺锤波振荡，在开启反应恢复后，要么恢复缓慢（G1和G2组），要么根本不恢复（G3组）。我们得出结论，有强有力的证据表明，在长时间全脑缺血后，丘脑中继神经元及其与体感通路中抑制性中间神经元的网络相互作用存在选择性易损性，从而导致丘脑 - 皮层分离。
