Nagai Y, Narumi S, Nagawa Y, Sakurada O, Ueno H, Ishii S
J Neurochem. 1980 Oct;35(4):963-71. doi: 10.1111/j.1471-4159.1980.tb07095.x.
Effects of TRH and pentobarbital alone, and in combination, on local cerebral glucose utilization of rats were studied by the autoradiographic 2-deoxy[14C]glucose method. TRH (5 mg/kg i.v.) reduced the rate of cerebral glucose utilization slightly in the whole brain. Locally, significant depression was observed in the following structures: frontal and visual cortices, hippocampus Ammon's horn and dentate gyrus, medial and lateral geniculate bodies, nucleus accumbens, caudate-putamen, substantia nigra, pontine gray matter, superior colliculus, superior olivary nucleus, vestibular nucleus, lateral lemniscus and cerebellar cortex. Pentobarbital (30 mg/kg i.v.) produced a marked and diffuse reduction in the rate of glucose utilization throughout the brain. TRH given 15 min after the administration of pentobarbital markedly shortened the pentobarbital sleeping time and caused some reversal of the depression in local cerebral glucose utilization produced by pentobarbital. These effects were almost completely abolished by pretreatment with intracerebroventricular injection of atropine methyl bromide (20 microgram/rat). These results indicate that although TRH acts to cause a reduction in the rate of cerebral glucose utilization, it reverses the depression induced by pentobarbital, via a cholinergic mechanism, in a number of structures, some of which are related to monoaminergic systems and the reticulo-thalamo-cortical activating system.
采用放射自显影2-脱氧[14C]葡萄糖法,研究了促甲状腺激素释放激素(TRH)和戊巴比妥单独及联合应用对大鼠局部脑葡萄糖利用的影响。静脉注射TRH(5mg/kg)可使全脑的脑葡萄糖利用率略有降低。在局部,以下结构观察到明显的抑制:额叶和视觉皮层、海马角和齿状回、内侧和外侧膝状体、伏隔核、尾状核-壳核、黑质、脑桥灰质、上丘、上橄榄核、前庭核、外侧丘系和小脑皮层。静脉注射戊巴比妥(30mg/kg)可使全脑葡萄糖利用率显著且广泛降低。戊巴比妥给药15分钟后给予TRH可显著缩短戊巴比妥睡眠时间,并部分逆转戊巴比妥引起的局部脑葡萄糖利用抑制。预先经脑室内注射甲基溴化阿托品(20μg/大鼠)可几乎完全消除这些作用。这些结果表明,尽管TRH可降低脑葡萄糖利用率,但它通过胆碱能机制在一些结构中逆转戊巴比妥诱导的抑制,其中一些结构与单胺能系统和网状-丘脑-皮质激活系统有关。