Projections from the lateral geniculate nucleus in the cat and monkey

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688M. E. WILSON AND B. G. CRAGGDISCUSSIONIn the monkey, our first lesion destroyed the postero-dorsal pole of the LGN, andproduced cortical fibre degeneration in the antero-ventro-lateral corner of the striatecortex in the angle between the lunate and inferior occipital sulci. This result isconsistent with previous work, for Clark & Penman (1934) found that a lesion in themacular part of the retina produced transynaptic neuronal atrophy in the posterodorsalpole of the LGN, and Talbot & Marshall (1941) recorded electrical responsesin the antero-ventro-lateral part of the striate cortex to photic stimulation of themacula. Degenerated fibres in the striate cortex after lesions in the LGN were notconcentrated in the stria of Gennari, and this is consistent with the preservation ofthe latter after undercutting the striate cortex, as found by Clark & Sunderland(1939). In both our monkeys with LGN lesions, fibre degeneration in the striate areaextended to the boundary of areas 17 and 18. Myers (1965) showed that this part ofthe striate area is connected to the adjacent part of area 18. The abrupt cessation ofthe degeneration at the boundary of area 17 with area 18 was thus convincingevidence that the LGN in the monkey does not project into the appropriate part ofarea 18. Fibre degeneration was, moreover, absent from the rest of areas 18 and 19.Our results in the cat show that the striate area receives a topographically organizedprojection from the LGN, e.g. medial lesions in the latter produce fibre degenerationin the lateral edge of area 17, while a lateral lesion (C9) caused fibre degenerationdeep in the medial wall of the lateral gyrus (see Fig. 7). The rostro-caudal arrangementis consistent with the results of earlier workers who studied the location of retrogradedegeneration in the LGN after making lesions in parts of the lateral gyrus (Minkowski,1913; Waller & Barris, 1937). The mapping of the visual field by electrophysiologicalmethods in the LGN (Seneviratne & Whitteridge, 1962; Bishop, Kozak, Levick &Vakkur, 1962) and on the visual cortex (Talbot & Marshall 1941; Bilge, Seneviratne &Whitteridge, 1963) again implies the same topographical relationship between theLGN and the visual cortex.Our finding in the cat of a second projection from the LGN that supplies afferentsto area 18 was unexpected, although this area was known to contain a second topographicalrepresentation of the visual field (Visual II) as shown by Talbot (1942)and Bilge, Seneviratne & Whitteridge (1963). Indeed Talbot (1942) suggested thatVisual IIreceived an independent projection from the LGN, for the responses therewere not 'depressed by narcosis or cautery of the lateral gyrus', and were 'independentof convulsants applied at the medial locus'. Moreover, Doty (1958) was able torecord photic responses from the lateral half of the lateral gyrus after the moremedial area had been removed. However, removal of the middle of the lateral gyrus(containing VisualII) produced only a small area of retrograde degeneration in themedial edge of the LGN. This degeneration was attributed to the lesion extendinginto the optic radiation running to the striate cortex (Doty, 1958).There is a possibility that the projection to Visual II degenerates after lesions in theLGN because of damage to fibres of extraneous origin which might pass through theLGN. There are however, two facts that make this explanation improbable: first,the disposition of the degeneration in Visual II is topographically organized in amanner complementary to that in Visual I (see Fig. 7), being thus compatible with
Projections from lateral geniculate nucleus689the mapping of the visual field in Visual II (Whitteridge, 1966). Fibres arising in moremedial structures and passing through the LGN towards the internal capsule wouldbe interrupted equally by medial or lateral lesions in the LGN, and would not thereforebe expected to show a topographical distribution related in the correct mannerto the position of the lesion in the LGN. Secondly, lesions have been made in thestructures surrounding the LGN medially, and the resulting cortical degenerationin the lateral part of the lateral gyrus only slightly overlapped that found in Visual IIafter LGN lesions, and never extended to the medial boundary of Visual II wherecentral vision is represented and where degeneration was found after lesions in themedial part of the LGN.These two arguments do not apply to the cortical degeneration seen in the suprasylviangyrus after LGN lesions, for this was also present after lesions in more medialstructures and did not show any marked topographical distribution. There is, however,independent electrophysiological evidence of a direct projection from the LGNto the suprasylvian gyrus (Vastola, 1961) which has been corroborated by the evidenceof Thompson, Smith & Bliss (1963). Buser, Borenstein & Bruner (1959) have shownthat a pathway via the thalamus medial to the LGN may be important for photicallyevokedresponses on the crown of the middle suprasylvian gyrus. They did not showthat this pathway is essential, and in any case they may have been dealing with anarea of the suprasylvian gyrus more medial than that implicated in our experimentswith the LGN lesions. Bruner (1965) has reduced but not abolished the photicallyevokedresponse in the lateral part of the middle suprasylvian gyrus by injectingpotassium chloride into the thalamus medial to the LGN. No studies of retrogradedegeneration in which only the middle suprasylvian gyrus was removed have beenreported. Marshall, Talbot & Ades (1943) in one cat removed the lateral gyrus onone side and, after allowing time for retrograde degeneration to occur, were unableto obtain the short latency response from the middle suprasylvian gyrus. It is unfortunatethat no histology was reported, as this result may imply that the middlesuprasylvian gyrus is supplied by collaterals of fibres to the lateral gyrus and thatthese collaterals are insufficient to sustain the parent-cell body when the main branchto the lateral gyrus is destroyed.In addition to these three projections from the LGN discussed above, we founddegenerated fibres in the lateral half of the lateral gyrus after lesions of structuresmedial to the LGN (Fig. 7). This cortical degeneration seemed to be mainly in area 19,or Visual III of Whitteridge (1966) and Hubel & Weisel (1965), with perhaps someextension into the lateral part of area 18 or Visual II. When degeneration was presentin the lateral part of the lateral gyrus, it also appeared at the bottom of the splenialsulcus. Although this degeneration extended some way along the upper wall of thesulcus, it was still more deeply situated than that caused by the most lateral lesionin the LGN. By analogy with the situation on the dorsal surface it would appearthat this is a projection to either area 18 or 19 related to the extreme periphery of thevisual field. Cytoarchitectonic studies of this region are conflicting: Winkler & Potter(1914) and Gurewitsch & Chatschaturian (1928) described an area 18 here, butOtsuka & Hassler (1962) distinguish area 18 only on the dorsal surface of the brain,and describe the region in the depth of the splenial sulcus as area 19. However, it isdifficult to imagine a Visual II or Visual III (area 18 or 19) in the splenial sulcus in43-2
Page 1 and 2: J. Anat. (1967), 101, 4, pp. 677-69
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Projections from the lateral geniculate nucleus in the cat and monkey

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