Expression of thymosin beta(4) messenger RNA in normal and kainate-treatedrat forebrain

Thymosin beta(4) is a major actin-sequestering peptide widely distributed i n mammalian tissues, including the nervous system. In the present study, we analyse the expression of thymosin beta(4) in normal and kainate-treated r at forebrain. In untreated animals, thymosin beta(4) messenger RNA is mainl y expressed in neurons of the hippocampal formation, neocortex and amygdalo id complex, as well as in oligodendrocytes. Other high-expressing areas are the tanycytic ependyma of the infundibulum, the substantia nigra pars comp acta, and the supraoptic and premammillary nuclei. In rats treated with kai nate, an excitotoxin that induces synaptic activation in the CA1-CA3 pyrami dal neurons of the hippocampus, the levels of thymosin beta(4) were clearly increased in the hippocampus and neocortex during the first 2-3 h after in jection. In the long term, kainate causes neuronal degeneration in the CA1- CA3 regions of the hippocampus and functionally related structures, provoki ng a depletion of thymosin beta(4) messenger RNA in these areas; however, t he levels of this transcript are restored two weeks after kainate injection . Moreover, we have found that, in these degenerating zones, gliosis is acc ompanied by an elevation of the levels of thymosin beta(4) messenger RNA, p articularly in the CA1-CA3 region of the hippocampus, the lateral geniculat e nucleus and the mammillothalamic tract. The present results demonstrate the existence of relatively high levels of thymosin beta(4) messenger RNA in several areas of the rat forebrain, indic ating that this peptide plays an important role in the regulation of actin polymerization in these regions of the brain. Moreover, the elevation of th is messenger RNA after kainate treatment suggests a function of thymosin be ta(4) in the production and remodelling of neuronal processes. Finally, our findings provide evidence for a participation of this actin-sequestering m olecule in the reactivity of certain types of glial cell that follows kaina te lesions. (C) 1999 IBRO. Published by Elsevier Science Ltd.