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The uptake of 6-H3 thymidine in the optic tectum and the forebrain of the newt following injury to one of the two nervous areas, shows a marked proliferative response in the telencephalon in the presence of a lesion on the right optic tectum, and a poor response of the optic tectum after a lesion on the right telencephalic lobe. A similar proliferative response is also obtained when the specimens received only the cold shock. In both experimental conditions maximum uptake is obtained after 7 days. It is assumed that the matrix cells of the forebrain and the undifferentiated cells of the optic tectum respond differently to the regeneration factor released by the nervous tissue following a lesion or a cold shock.

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.

A histochemical light and electron microscopy study of acetylcholinesterase (AChE) was carried out on the regenerating opic tectum of adult newt. A plug of optic tectum was removed and 15 days later [6-H3] thymidine was injected. Ninety days after the lesion the brain was removed, treated for histochemical AChE-detection and autoradiographic analysis. This double treatment showed the capacity of these adult amphibians to regenerate the nervous tissue through the proliferation of undifferentiated elements and their subsequent differentiation into neurons as is shown by the presence of cells both labelled by [6-H3] thymidine and by the AChE-reaction product.

The permeability of the newt cerebral capillaries to lanthanum ion has been studied after perfusion with mannitol solutions of increasing molarity. In the control specimens lanthanum deposits were limited to the luminal side of the capillaries and tracer did not spread to the pericapillary spaces due to the tight junctions. Treatment with hypertonic solutions of mannitol (0.25M, 0.5M, 1M) caused opening of the blood brain barrier with a progressive increase in lanthanum between the endothelial cell edges, in the basal lamina and in the extracellular spaces of the nervous parenchyma in relation to the molarity of the mannitol solution. The spread of lanthanum is probably due to opening of the tight junctions between the endothelial cells, since pinocytotic vesicles labelled with tracer were not evident.