Studies on cholecystokinin-containing neuronal pathways in rat cerebral cortex and striatum.
Lesion experiments were performed to investigate the origin of CCK-containing afferents of the striatum. All the subdivisions of the striatum that were investigated seem to receive CCK afferents from dorsolateral and lateral neocortical areas. However, destruction of these cortical areas alone did not reduce CCK-IRC in the striatum. Only after an additional parasagittal severance of the corpus callosum were significant decreases in CCK-IRC of all striatal subdivisions observed. Thus, CCK neurons in ipsilateral midline areas (such as the cingulate cortex) or, more likely, in contralateral cortical areas, seem to project to the striatum of one side. The CCK fibers seem to enter the striatum via the capsula externa, since a lesion of this structure has been shown to diminish the CCK-IRC in the striatum. In addition, the dorsomedial part of the head of the striatum may receive a projection of CCK fibers from the anterior cingulate area. A series of lesions which severed the afferents of structures caudal to the striatum, that is, the amygdaloid complex and the ventral tegmental area plus substantia nigra, did not reduce CCK-IRC in the striatum. Some of these lesions even significantly enhanced CCK-IRC in several subdivisions of the ipsilateral and contralateral striatum. Further studies will be necessary to cast some light on these caudal CCK afferents to the striatum, which are obviously extremely complex.
D000344:Afferent Pathways / Q000032:analysis; D000818:Animals; D002540:Cerebral Cortex / Q000032:analysis*; D002766:Cholecystokinin / Q000032:analysis* / Q000276:immunology; D003337:Corpus Callosum / Q000032:analysis; D003342:Corpus Striatum / Q000032:analysis*; D008297:Male; D009410:Nerve Degeneration; D009474:Neurons / Q000032:analysis*; D051381:Rats; D011919:Rats, Inbred Strains
D002766:Cholecystokinin