Tasaka K, Chung Y H, Mio M, Kamei C
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Okayama University, Japan.
Brain Res Bull. 1993;32(4):365-71. doi: 10.1016/0361-9230(93)90201-l.
Electrical stimulation (3 Hz, 0.5 volts) to the midbrain reticular formation of conscious rats induced significant increase of EEG power densities (synchronization) recorded at the frontal cortex (FCOR), nucleus ventralis thalami (VE), or nucleus medialis centralis thalami (CM). Significant synchronization was also observed in the FCOR when electrical stimulation was applied to the VE and CM. When ipsilateral and bilateral VEs were electrocoagulated, no EEG synchronization was observed in the FCOR and CM. Intracerebroventricular administration of histamine (Hi) caused a marked suppression of FCOR EEG synchronization in both CM-lesioned and normal rats through H1 receptors. EEG synchronization in FCOR was not induced in ipsilateral or bilateral VE-lesioned rats after RF stimulation. When Hi (1 microgram) was injected into the VE of normal rats, EEG synchronization of FCOR was markedly reduced after RF or VE stimulation. No such changes were induced when Hi was injected into the CM.
对清醒大鼠的中脑网状结构进行电刺激（3赫兹，0.5伏），可使额叶皮质（FCOR）、丘脑腹侧核（VE）或丘脑中央内侧核（CM）记录到的脑电图功率密度显著增加（同步化）。当对VE和CM进行电刺激时，在FCOR中也观察到显著的同步化。当同侧和双侧VE被电凝时，在FCOR和CM中未观察到脑电图同步化。脑室内注射组胺（Hi）通过H1受体在CM损伤和正常大鼠中均引起FCOR脑电图同步化的显著抑制。射频刺激后，同侧或双侧VE损伤的大鼠未在FCOR中诱导出脑电图同步化。当向正常大鼠的VE中注射Hi（1微克）时，射频或VE刺激后FCOR的脑电图同步化明显降低。当向CM中注射Hi时未诱导出此类变化。
