Distinct neurochemical populations in the rat central nucleus of the amygdala and bed nucleus of the stria terminalis: Evidence for their selective activation by interleukin-1 beta

The lateral division of the central nucleus of the amygdala (CEA1) and the oval nucleus of the bed nucleus of the stria terminalis (BSTov) have been l inked closely anatomically and functionally. To determine whether these reg ions may be subdivided further on a neurochemical basis, dual in situ hybri dization was used to determine the colocalization of corticotropin-releasin g hormone (CRH), enkephalin (ENK), or neurotensin (NT) with glutamic acid d ecarboxylase isoforms 65 and 67 [used concurrently as a marker for gamma-am inobutyric acid GABA] in these nuclei. It was found that, for both regions, each peptide invariably was localized in a GABAergic cell. Although there was a similar overlap in the distribution of NT with ENK in the BSTov and C EAl, it was observed that CRH and ENK rarely were colocalized in either nuc leus. To determine whether these distinct neuronal populations could be act ivated differentially, male rats were given a systemic injection of interle ukin-1 beta (IL-1 beta; 5 mu g/kg, i.p.), a stimulus that results in a robu st increase in c-fos mRNA expression in the BSTov and CEA1. The neurochemic al identity of these activated neurons showed striking similarities between the BSTov and the CEAl; All IL-1 beta-responsive cells were GABAergic, the majority of c-fos- positive cells expressed ENK mRNA (BSTov, 81%; CEA1, 94 %), and some expressed NT mRNA (BSTov, 23%; CEAl, 22%), whereas very few ex pressed CRH mRNA(BSTov, 4%; CEAI, 1%). These data provide evidence for the existence of discrete neural circuits within the BSTov and CEAI, and the si milarities in the patterns of neurochemical colocalization in these nuclei are consistent with the concept of an extended amygdala. Furthermore, these data indicate that intraperitoneal IL-1 beta recruits neurochemically dist inct pathways within the BSTov and CEA1, and it is suggested that this diff erential activation may mediate specific aspects of immune, limbic, and/or autonomic processes. J. Comp. Neurol. 413:113-128, 1999. (C) 1999 Wiley-Lis s, Inc.