Regional distribution of cholecystokinin receptors in macaque medial temporal lobe determined by in vitro receptor autoradiography.

Abstract

Cholecystokinin (CCK) binding sites were localized in the hippocampus, amygdala, and medial temporal cortices of macaque monkeys by using techniques of in vitro receptor autoradiography. Binding sites were labeled with 3H-CCK-8 and 125I-CCK-33, and nonspecific binding was assessed in the presence of 1 microM CCK-8. Comparison of autoradiograms with Nissl-stained sections allowed precise correlation of autoradiographic grain distribution with cytoarchitecture. CCK binding in the amygdala varied among nuclear subdivisions. It was dense in the lateral, basomedial, endopiriform, and cortical nuclei, in the parvicellular portion of the accessory basal nucleus, the periamygdaloid cortex, the cortical transition area, and in the amygdalohippocampal area. Labeling was sparse in the central, medial, and basolateral nuclei as well as in the magnocellular accessory basal nucleus. In the hippocampal formation, a single dense band of CCK binding was observed over the granule cell layer and adjacent few millimeters of the molecular layer of the dentate gyrus, while in the polymorph and remaining portions of this layer binding was of very low density. Prominent label over the pyramidal layer in the presubiculum clearly distinguished this region from the adjacent subiculum in which binding just exceeded background levels. Moderate to light label was observed in the hilus and stratum pyramidale of CA3, CA2, and CA1, while other hippocampal layers showed minimal specific binding. Variation in CCK binding in the medial temporal cortex showed close correspondence to cytoarchitectonic subdivisions. In entorhinal cortex, for example, binding was concentrated in layers III-VI while label in area 35 was prominent in all laminae except layer IV. Area TH of von Bonin and Bailey ('47) was distinguished from other regions by evenly distributed binding across all layers, while in area TF a bilaminar pattern of label in layers II and IV was observed. The highly specific patterns of CCK binding in amygdala and transitional cortices of the medial temporal lobe can be related to terminal fields of neo- and allocortical afferents to these regions, while label in the hippocampal formation coincides with the terminals of intrinsic neurons which ramify among the somata of cells that are targets of neocortical afferents. Thus, in all structures of the medial temporal lobe the disposition of peptidergic binding sites suggests that CCKergic systems may be important in the modulation of cortical afferents.