Alterations in local cerebral glucose utilization during chronic treatment with an ACTH 4–9 analog

Abstract

Adrenocorticotrophic hormone (ACTH) and structural analogs of the fragment ACTH 4–9 have marked effects upon behaviour (particularly in relation to memory processes). The effects of the chronic (10 day) administration of the potent analog [Met(O 2) 4, D-Lys 8, Phe 9]ACTH 4–9 (100 μg/kg per day i.p.) upon local cerebral glucose utilization have been examined using the autoradiographic 2-deoxyglucose technique in an attempt to identify the neuroanatomical sites involved functionally in the central actions of this ACTH 4–9 analog. Of the 49 anatomically discrete regions examined, significant increases in glucose utilization were observed only in the hippocampus (stratum moleculare lacunosum and parasubiculum, increased by 16 and 17% respectively), the anterior nucleus of the thalamus (by 23%) and anterior cingulate cortex (by 30%). The highly localized alterations in glucose utilization which were observed following treatment with this ACTH 4–9 analog provide evidence for the functional involvement of a hippocampal—anterior thalamic—anterior cingulate cortical circuit in the actions of this peptide fragment.