Projections from the lateral geniculate nucleus in the cat and monkey

690M. E. WILSON AND B. G. CRAGGthe topographical scheme proposed by Whitteridge (1966). The alternative hypothesisthat the degeneration in the splenial sulcus lies in Visual I cannot be supportedeither for topographical reasons, even allowing that there may be no representationof central vision in the medial interlaminar nucleus (Stone & Hansen, 1966). A thirdpossibility is that the degeneration in the splenial sulcus is neither in Visual I, IInor III, but in some other cytoarchitectonic area, perhaps cingulate cortex.The exact origin of this projection from structures medial to the LGN is uncertain.The relevant lesions always involved the medial interlaminar nucleus, but also extendedinto adjacent parts of the pulvinar nucleus. One medially placed lesion (C 15)was restricted to the pulvinar, lateralis dorsalis and lateralis posterior nuclei, andcortical-fibre degeneration was confined to the middle suprasylvian gyrus (see Fig. 7).Garey (1965) has reported retrograde degeneration in the medial interlaminar nucleusfollowing cortical lesions placed lateral to area 17 of Otsuka & Hassler (1962). Theseresults suggest that the medial interlaminar nucleus may be the origin of the projectionto the lateral part of the lateral gyrus (Visual III), but we cannot exclude thepossibility that the most medial part of the pulvinar nucleus untouched by the lesionin C 15 might also project to Visual III. Whether the medial interlaminar nucleushas an independent projection to the suprasylvian gyrus could not be determined.The brief report by Garey (1965) also states that the LGN projects ipsi-laterally toareas 17-19, but it is not clear whether the medial interlaminar nucleus is includedin this statement.We found no evidence of a contra-lateral cortical projection from the LGN ineleven cats and two monkeys. The contrary result by Glickstein, Miller & Smith(1964) is perhaps attributable to their approach through the corpus callosumdamaging transcallosal fibres interconnecting the visual areas of cortex. As thesingle control lesion reported by these authors was ventral to the LGN, it is probablethat the track was anterior to that used in the other experiments, and might thushave missed the forward edge of the relevant transcallosal fibres.SUMMARY1. A stereotaxic approach to the thalamus was designed to avoid the corpuscallosum. An adaptation of the Nauta-Gygax method to batch-staining that preservedserial order and avoided the handling of individual sections is described.2. Stereotaxic lesions were placed in the LGN of two monkeys. Fibre degenerationwas confined to the ipsi-lateral striate cortex and ceased abruptly at the end of thestria of Gennari.3. Stereotaxic lesions were made wholly within the LGN in three cats. There weretwo areas of fibre degeneration within the lateral gyrus corresponding to Visual I andVisual II (areas 17 and 18) and one on the lateral wall of the middle suprasylviangyrus. The degeneration in the first two areas was topographically organized.4. Stereotaxic lesions were made in thalamic structures medial to the LGN inthirteen cats. The medial interlaminar nucleus of the LGN was damaged in elevencats, three of which had no damage in the main body of the LGN. Fibre degenerationwas found on the lateral edge of the lateral gyrus, probably in area 19 (Visual III)and also in the depth of the splenial sulcus. There was no indication that accidental