Brain Research, 307 (1984) 201-215 201 Elsevier BRE 10236 Deafferentation and Axotomy of Neurons in Cat Striate Cortex: Time Course of Changes in Binocularity Following Corpus Callosum Transection B. R. PAYNE, H. E. PEARSON* and N. BERMAN Departments of Anatomy and Physiology~Biochemistry, The Medical Collegeof Pennsylvania, EPPI Division, Philadelphia, PA 19129 (U.S.A.) (Accepted January 17th, 1984) Key words: corpus callosum transection - - deafferentation - - axotomy - - area 17 - - ocular dominance - - cat Single neurons were recorded in the eallosal terminal and cell zones of area 17 in the cat to assess the time course of changes in the proportion of binocular neurons produced by corpus callosum transection. The callosal terminal zone contains all the degenerating terminals in area 17 after corpus callosum transection. The callosal cell zone contains all the cells in area 17 which contribute axons to the corpus callosum. The cell zone is larger than, and partially overlaps, the eallosal terminal zone. After corpus callosum transection there was an initial change in ocular dominance of neurons in both caUosalzones. This initial change was followed by a reduction in the proportion of binocular neurons in both zones. This reduction became maximal 2-4 weeks after transection. In the callosal terminal zone, binocularity did not recover even at the longest postoperative periods examined (31-42 weeks). In the part of the callosal cell zone outside of the callosal terminal zone, the proportion of binocular neurons began to recover after 5 weeks and was at normal levels at the longest survival periods studied. Corpus callosum transection deafferents and axotomizes cells in the callosal terminal zone and, since central neurons do not regenerate their long-ranging axons, the combined effects of deafferentation and axotomy in this zone are permanent. The callosal cell zone outside of the callosal terminal zone contains axotomized cells and no degenerating terminals fol- lowing transection. The recovery of binocularity in this region may be attributed to the transient changes which axotomized cells un- dergo. The zone which contains no callosal cells or terminals is unafected by transection of the corpus callosum. INTRODUCTION Area 17 of cat cerebral cortex is connected recip- rocally with a number of contralateral visual areas via the corpus callosum46,s0,53,63, 64. Area 17 is highly or- ganized in terms of its caUosal connections, which makes the callosal system in area 17 ideal for study- ing the retrograde consequences of axon damage alone, or in combination with deafferentation, in the specific callosal subdivisions of area 17. These subdi- visions of area 17 can be defined on the basis of the anatomical location of cells which receive terminals from axons originating in the contralateral hemi- sphere and of cells which send axons to the contralat- eral hemisphere (Fig. 1). The callosal terminal or re- cipient zone is adjacent to the border with area 18 and contains all the terminals of callosal axons which project to area 17. The callosal cell zone is larger than the terminal zone and also lies adjacent to the border with area 18. While overlapping partially with the terminal zone, the callosal cell zone also includes more medial regions of cortex which contain callosal- ly projecting cells. The third zone, referred to as acal- losal, occupies the remainder of area 17 and contains no callosal cells or callosal terminals. Because of the arrangement of these caUosal zones, transection of the corpus callosum deafferents cells in the callosal terminal zone and axotomizes callosal cells in the cal- losal cell zone. Therefore, the effects of corpus callo- sum transection on cells in the callosal terminal zone may include both deafferentation and axotomy. In the region of the callosal cell zone medial to the ter- minal zohe, cells are only axotomized. Medial to the callosal cell zone, cells are neither deafferented or axotomized. Our previous studies have shown that disruption of * Present address: Department of Anatomy; Temple University Medical School, 3400 N. Broad Street, Philadelphia, PA 19140, U.S.A. Correspondence: B. R. Payne, Department of Anatomy, The Medical College of Pennsylvania, 3200 Henry Avenue, Philadelphia, PA 19129, U.S.A. 0006-8993/84/$03.00© 1984 Elsevier Science Publishers B.V.