The organization of the corticocuneate pathway was investigated in monkeys by using the anterograde and retrograde axonal transport of either horseradish peroxidase (HRP) or wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). Injection of either tracer into the precentral cortex (centered on area 4) results in heavy anterograde labeling in the tegmental region, which lies immediately ventrolateral to the cuneate nucleus, particularly at levels caudal to the obex. On the other hand, injections of the same tracers involving areas 3b, 1, and 2 cause anterograde labeling mainly within the core (pars rotunda of Ferraro and Barrera, '35, Arch. Neurol. Psychol. 33:262-75) of the cuneate nucleus. Anterograde labeling is also evident in the rostral parts of the cuneate nucleus, especially after injections involving areas 1 and 2. Injections restricted largely to area 3b cause anterograde labeling preferentially in the core of the cuneate nucleus. After injection of HRP or WGA-HRP into the dorsal medulla, retrogradely labeled neurons are present both in the pre- and postcentral gyrus, but their location depends upon the sites and extent of the injection site. When the tracer diffuses into the underlying tegmental area, many retrogradely labeled neurons appear in the precentral motor cortex, principally in area 4 although some of them also occur in area 6. With smaller injections, largely restricted within the cuneate nucleus, most labeled neurons are present in the postcentral gyrus, with the largest population in areas 1 and 2; a smaller number of small neurons in area 3b are best demonstrated with WGA-HRP; and area 3a contains the smallest complement of retrogradely labeled neurons. The data from these studies suggest a segregation of pre- and postcentral afferents in the ventral tegmental region and the cuneate nucleus, respectively. These findings pertaining to the corticocuneate projection in the monkey are discussed in relation to the parallelism between monkeys and cats possible physiological implications of the anatomical organization described, and conflicting evidence in the neurophysiological observations obtained, by earlier investigators, by antidromic and orthodromic activation of this pathway.