Caminiti R, Innocenti G M
Exp Brain Res. 1981;42(1):53-62. doi: 10.1007/BF00235729.
The distribution of S1 (first somatosensory area) and S2 (second somatosensory area) neurons projecting to the contralateral S2 was studied with horseradish peroxidase in normal adult cats and in cats aged between 129 and 248 days in which the injected S2 area had been deprived of some of its input by an earlier lesion (on postnatal days 3 to 30; day of birth = day 1) of ipsilateral S1, alone or combined with a lesion of contralateral S2. In animals with S1 lesions, as in the normal controls, labeled neurons were selectively distributed to the regions of the trunk representation and to parts of the forelimb and hindlimb representations; however, the normally acallosal region in the forepaw representation contained scattered labeled neurons in three of the four animals whose S1 had been lesioned during the first postnatal week. In these animals, the distribution of labeled neurons in the contralateral S2 was apparently normal. Furthermore, the additional lesion of this area during the first postnatal week (one animal) did not increase the degree of filling-in of the normally acallosal parts of S1. The partial filling-in of the acallosal parts of S1 is probably due to the preservation to adulthood of some of the callosal neurons which are present in these regions during the early postnatal life. Possibly, these neurons did not disappear (or lose their callosal axons) because the neonatal lesion (i) allowed their successful competition for terminal space in contralateral S2 or (ii) induced a reorganization of the peripheral input to this area.
运用辣根过氧化物酶,研究了正常成年猫以及出生129至248天的幼猫中,投射至对侧S2区的S1(第一体感区)和S2(第二体感区)神经元的分布情况。在这些幼猫中,同侧S1区在出生后第3至30天(出生日为第1天)单独或联合对侧S2区受损,致使注射的S2区部分输入缺失。与正常对照组动物一样,在S1区受损的动物中,标记神经元选择性地分布于躯干代表区以及部分前肢和后肢代表区;然而,在出生后第一周内S1区受损的四只动物中的三只,其前爪代表区正常的无胼胝体区域含有散在的标记神经元。在这些动物中,对侧S2区标记神经元的分布显然正常。此外,在出生后第一周对该区域进行额外损伤(一只动物),并未增加S1区正常无胼胝体部分填充的程度。S1区无胼胝体部分的部分填充可能是由于出生后早期生活中存在于这些区域的一些胼胝体神经元保留至成年。这些神经元可能没有消失(或失去其胼胝体轴突),原因可能是:(i)新生儿损伤使其成功竞争对侧S2区的终末空间;或者(ii)诱导了该区域外周输入的重组。