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Homotopic transplant of fetal cortex to lesioned motor cortex of adult rats. A comportamental and anatomical study.

F. Cicirata, M. F. Serapide, G. Nicotra, R. Raffaele


Previous investigations have shown that the transplant of fetal nervous tissue in adult, formerly injured, brain induces an improvement of the neurological deficits. The process underlying this finding is not yet known. It has been proposed that this process is favourably supported by the reconstruction of the damaged circuitry, replacing the injured neurons with the transplanted fetal cells. In the present study we have investigated the relation between the improvement of the neurological deficits and the anatomical integration of the transplanted neurons within the host brain. The plan of the investigation included two steps: the first step consisted of inducing neurological deficits by kainic acid lesion of the motor cortex and then studying the changes in the motor learning following a homotopic transplant of fetal cortex in the side of the lesion. The second step consisted of studying the anatomical integration of the transplanted cortex with the thalamus of the host. The results showed that the rats with injury of the motor cortex followed by solid transplant of fetal cortex (E 17) had a significantly greater recovery of the motor learning with respect to non-transplanted rats with a lesioned motor cortex. In the same rats, the connections between the transplanted cerebral cortex and the thalamus of the host has been investigated. WGA-HRP solution was injected in the thalamus and both labeled fiber terminals and labeled cells were searched for in the transplants. The results showed that: 1) the host thalamus projects to the transplanted cortex with a lower density than to the host cortex surrounding the transplant; 2) the thalamic projection to the host cortex is topographically organized, whereas the projection to the transplant is arranged in patches without any topographical organization; 3) the transplant does not send a significant projection to the thalamus of the host. In conclusion, the experimental findings demonstrate that the reconstruction of an injured thalamo-cortical circuitry of adult rats transplanting fetal neurons is not possible. The improvement of the functional deficits by the transplant of fetal tissue may be referred to aspecific factors enhancing the functional activity of the host cortex undamaged by the initial injury. The identification of the nature of the hypothesized factors requires further investigation.

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