Effect of Thyrotropin‐Releasing Hormone (TRH) on Local Cerebral Glucose Utilization, by the Autoradiographic 2‐Deoxy[14C]glucose Method, in Conscious and Pentobarbitalized Rats

Publisher Website
Google Scholar
Abstract
Effects of TRH [thyrotropin releasing hormone, thyroliberin] 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 pentobarbital administration 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 .mu.g/rat). TRH acts to cause a reduction in the rate of cerebral glucose utilization, but it apparently reverses the depression induced by pentobarbital, via a cholingeric mechanism, in a number of structures, some of which are related to monoaminergic systems and the reticulo-thalamo-cortical activating system.