Alterations in local cerebral glucose utilization following central administration of corticotropin-releasing factor in rats.

Abstract

We have examined the effects of intracerebroventricular administration of corticotropin-releasing factor (CRF) (5.25 nmol in 10 microliters of saline) on glucose utilization, an index of cerebral function, in 65 anatomically discrete regions of rat brain by using the 14C-2-deoxyglucose quantitative autoradiographic technique. CRF administration increased plasma glucose concentrations with a temporal onset and magnitude of response similar to those previously reported. CRF differentially affected glucose utilization (GU) in discrete regions of rat brain. Consonant with the hypophysiotropic role for CRF, pronounced increases in GU were seen in median eminence and lateral nucleus of the hypothalamus. CRF also increased GU in brain regions implicated in mediating responses to stress including locus coeruleus and median raphe nucleus. In contrast, reductions in GU were observed in prefrontal cortex and nucleus accumbens. Punctate increases in GU were noted in the cerebellar cortex. Furthermore, large increases in GU occurred in vermis, inferior olive, and red nucleus substantiating a neurotransmitter role for CRF in the olivocerebellar pathway. Additional brain areas showing significant alterations in GU in response to CRF included anteroventral, anterior pretectal, and posterolateral nuclei of the thalamus, fornix, dorsal tegmental nucleus, spinal trigeminal nucleus, and cuneate nucleus. These data demonstrating regional changes in GU in response to CRF administration further elucidate the neuroanatomical substrates underlying the actions of CRF in brain and support the role of this neuropeptide in coordinating responses to stress.