Churchill Lynn, Yasuda Kyo, Yasuda Tadanobu, Blindheim Kelly A, Falter Michael, Garcia-Garcia Fabio, Krueger James M
Department of VCAPP, College of Veterinary Medicine, Washington State University, PO Box 646520, Pullman, WA 99164-6520, USA.
Brain Res. 2005 Sep 7;1055(1-2):15-24. doi: 10.1016/j.brainres.2005.06.052.
A unilateral microinjection of tumor necrosis factor alpha (TNFalpha) (150 ng) onto the primary somatosensory cortex induces state-dependent asymmetries in electroencephalographic (EEG) slow wave activity during non-rapid eye movement sleep in rats [H. Yoshida, Z. Peterfi, F. Garcia-Garcia, R. Kirkpatrick, T. Yasuda, J.M. Krueger, State-specific asymmetries in EEG slow wave activity induced by local application of TNF alpha, Brain Res. 1009 (2004) 129-136]. In the current study, analogous TNFalpha injections were performed to determine Fos- and interleukin-1beta (IL1beta) immunoreactivity (IR). A unilateral microinjection of TNFalpha increased the number of Fos- and IL1beta-IR cells in the primary somatosensory cortex relative to the contralateral side that received heat-inactivated TNFalpha. These asymmetric TNFalpha-induced increases in the number of Fos- and IL1beta-IR cells were evident along the outside surface of the cortex (mainly layers II and III) in a restricted rostral to caudal zone. Asymmetrical increases in the number of Fos-IR cells were also observed in the subcortical region that receives the main cortical projection from the somatosensory cortex, the somatic region of the reticular nucleus of the thalamus (reticular thalamus). The IL1beta-IR cells double-labeled with glial fibrillary acidic protein (GFAP), suggesting that many of the IL1beta-IR cells were astrocytes. The number of the IL1beta-IR cells in the reticular thalamus increased significantly ipsilateral to the TNFalpha injection. Current results indicated that Fos- and IL1beta-IR may be utilized to study the functional neuroanatomy involved in the TNFalpha-mediated state-dependent enhancement of EEG slow wave activity.
向大鼠的初级体感皮层单侧微量注射肿瘤坏死因子α（TNFα）（150纳克）会在非快速眼动睡眠期间诱导脑电图（EEG）慢波活动出现状态依赖性不对称[H. 吉田、Z. 彼得菲、F. 加西亚 - 加西亚、R. 柯克帕特里克、T. 安田、J.M. 克鲁格，局部应用TNFα诱导的EEG慢波活动的状态特异性不对称，《脑研究》1009（2004）129 - 136]。在当前研究中，进行了类似的TNFα注射以确定Fos和白细胞介素 - 1β（IL1β）免疫反应性（IR）。相对于接受热灭活TNFα的对侧，单侧微量注射TNFα增加了初级体感皮层中Fos和IL1β免疫反应性细胞的数量。这些TNFα诱导的Fos和IL1β免疫反应性细胞数量的不对称增加在皮层外表面（主要是II层和III层）沿头端至尾端的受限区域很明显。在接受体感皮层主要皮层投射的丘脑网状核的躯体区域（丘脑网状核）的皮层下区域也观察到Fos免疫反应性细胞数量的不对称增加。IL1β免疫反应性细胞与胶质纤维酸性蛋白（GFAP）双标，表明许多IL1β免疫反应性细胞是星形胶质细胞。TNFα注射同侧的丘脑网状核中IL1β免疫反应性细胞的数量显著增加。当前结果表明，Fos和IL1β免疫反应性可用于研究参与TNFα介导的EEG慢波活动状态依赖性增强的功能性神经解剖学。
