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The telencephalic proliferative response has been studied in adult newts after lesion on the central nervous system. Both in the animals injured on the optic tectum and in those on the telencephalon a telencephalic proliferative response was observed, localized in the dorsal pallial areas and in the striatum. Quantitative analysis of the proliferative activity of the matrix cells present in the telencephalon showed a different response pattern. In the animals lesioned on the telencephalon the labelled cells are much more numerous in the injured hemisphere than in the healthy one and these cells persists at a high level even in the specimens fixed 90 days after the lesion. In this case no labelled cells are observed in the midbrain. The number of labelled cells in the animals lesioned on the optic tectum was identical in both telencephalic hemispheres; this number decreases from 15 to 30 days after the injury and at 90 days labelled cells are not observed. These data confirm the presence of a neuronotrophic factor released in the ependymal fluid and active on the telencephalic periventricular matrix cells but not on the undifferentiated cells of the grey layers of the optic tectum. It is also assumed that the proliferation of matrix cells of an injured area causes the formation of glial cells and neurons, such proliferation in an intact zone is oriented to differentiation of glial cells alone.

The localization and proliferative response of optic tectum matrix cells has been studied in adult newt following an experimental lesion on an optic lobe. The results show that 15 days after the lesion the cells in division, autoradiographically labelled, are located in the periventricular layer. Thirty days after the lesion the labelled cells are also found in the innermost grey layers; at 90 days the injured optic tectum regains the cytoarchitecture characteristic of this centre, with labelled cells, whether in the external or in the internal pyriform layers. In all the stages the labelled cells are also found in the periventricular layers of the controlateral optic tectum, in the dorsal pallium and in the striatum. The quantitative data exhibit the existence of a direct relationship between the number of proliferating cells in the injured optic lobe and the extent of the lesion. These data show the possibility of active cellular proliferation for the reconstruction of the lesioned nervous area and for restoration of the characteristic histological structure.

The authors removed a simple plug from the dorsal hippocampus, or from the dorsal hippocampus and part of the medial hippocampus in a telencephalic hemisphere in specimens of Lacerta viridis. The specimens were sacrificed some time after the operation after administration of 6-3 H thymidina. The examination of the emulsified slides showed that in these experimental condition no reparative process is observed, except for an impressive proliferation of cells and fibres which, from the meninx, bridges the cortical gap and, penetrating the telencephalic ventricle, attaches itself to the surrounding nerve tissue. The authors also described a limited cellular proliferation in the ependima of the telencephalic ventricles as a result of resection of the medial hippocampus; this observation is interpreted as a phenomenum connected to compensatory hypertrophy.

The authors removed from Lacerta viridis specimens part of the dorsal hippocampus of one telencephalic hemisphere. The animals were sacrificed 110 and 260 days after the operation; 24 hours before the operation on the encephalon, each was dosed with 6--3H thymidine. An examination of the historadiographic slides showed a clear remedial process in the operated area which, 260 days after has renewed in thickness but was still minus its characteristic cellular layer. The area of the telencephalon affected by the remedial process was examined by the authors and they have put forward the hypothesis that in relation to the type of operation performed, said area is localized prevalently in the dorsal hippocampus of the caudal half of the telencephalic hemispherg. The authors have also shown that the remedial procress, though attenuated is still in progress. 260 days after the operation.

After keeping specimens of Rana esculenta at 4 degrees C for 24 hrs., the Authors removed a plug of right optic tectum. Thirty days later they injected 6-H3 thymidine and on the 200th day after surgery sacrificed the animals. With this technique it is possible to show the high regenerative capacity of the optic tectum; in fact, it is possible to observe reconstruction of the typical cellular and fibre layers of the removed nervous area. The origin of the cellular elements which supported this regenerative process and the possible connection between these results and restoration of the hemotrophic embryonic conditions due to absence of the blood-brain barrier, consequent on the cold treatment, is discussed.

To identify the nature of the dividing cells during the regenerative process of the telencephalon, the authors administered nerve growth factor (NGF) to Lacerta viridis with a wedge of telencephalon removed. Some known centers of cell proliferation were unresponsive to the treatment, whereas the ventral end of the telencephalic ventricle underwent an increase of up to 200% in proliferation rate. On the basis of this observation and data in the literature, the authors propose that the cell proliferation beginning in the medial area during the regeneration of the telencephalic ventricle is due to catecholaminergic neuroblasts still present in the adult.