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The present study investigates the development of microglial and astroglial cells in the postnatal rat striatum, using immunohistochemical methods with panel antibodies that recognize macrophage antigens of unknown function - ED l, complement type 3 receptor- OX-42 (for microglia) and glial fibrillary acidic protein (for astrocytes). On the day of birth, EDl/OX-42- immunoreactive microglial cells present in the striatum represent ameboid microglia. Between PO and P10 we could observe the migration of ameboid microglial cells from neuroepithelial ventricular zone through internal and external capsules into the striatum. During the second postnatal week (PIO, P14) a considerable decline of ameboid EDl-immunoreactive microglial cells and an increase of the number of OX-42 positive ramified cells were observed. At P21 only OX-42 positive ramified cells were observed in the whole striatum. On the day of birth, only a few GFAP positive cells resembling radial glia were observed in the striatium. During the first postnatal week, the number of GFAP-positive cells increased significantly; they showed typical morphology of the astrocytes present in the adult animals. After P22 the final striatal population of astroglia was formed.
Propofol can be potentially beneficial in oxidative stress related malignancies as neurodegenerative diseases and traumatic brain injury but its signalling pathways are poorly understood. In this study effect of propofol on astroglial signalling in oxidative stress was evaluated. Ten days old cultures of rat astroglial cells were treated for 1 hour with t-butyl hydroperoxide (tBHP) to induce oxidative stress following by 1 hour propofol. We measured cytotoxicity, changes in cell growth and apoptosis as well as alterations in expression and acetylation of chromatin core H3 and H4 histone proteins and changes in native and phosphorylated cAMP-response-element-binding protein (CREB). tBHP induced limited cytotoxicity, increased apoptosis, decreased glutamine synthetase and enolase activities, decreased nuclear CREB, CREB-P and histone proteins but unchanged cytosolic CREB and histone acetyltransferase (HDAC) expression. Propofol clearly protected the cells against tBPH-induced toxicity, normalized alterations in cell growth, restored to some extent glial enzyme activities and reduced apoptotic cell numbers. Also, propofol restored H3 but not H4 expression/activation, but was without effect on decreased nuclear CREB expression/activation. These data show that oxidative stress in cultured astroglia significantly affects nuclear CREB and histone proteins and point to the protective role of propofol.
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