DIMINISHED EXPRESSION OF MICROTUBULE-ASSOCIATED PROTEIN (MAP-2) AND BETA-TUBULIN AS A PUTATIVE MARKER FOR ISCHEMIC-INJURY IN NEOCORTICAL TRANSPLANTS

The present study examined the immunoexpression of the neuronal cytosk eletal proteins, MAP-2 and beta-tubulin within a timed series of rat f etal neocortical transplants. beta-tubulin is a major component of mic rotubules and MAP-2 regulates the assembly and stability of neuronal m icrotubules and is a major site for the phosphorylation cAMP dependent protein kinase in neurons. Both proteins are strongly expressed in th e soma and dendrites of normal neurons. MAP-2 has been shown to be a s ensitive marker for ischemia in neurons and is downregulated in this f orm of injury. Immunoexpression of both MAP-2 and beta-tubulin in graf ted cortical neurons was markedly reduced when compared to age-matched or even perinatal specimens at all post-operative times. Dendritic st aining was confined to random, thin processes with no laminar patterns and staining within somata was very weak. In some specimens, somatic expression was increased and dendrites were more robustly stained when a portion of the graft was juxtaposed to a fiber tract even though in other regions of the same graft there was very weak immunostaining. T he present results corroborated previous studies of cortical transplan ts in indicating an immature structure and metabolism, and it is sugge sted here that the primary factor is a sublethal form of ischemic inju ry. Another possibility for the relative paucity of cytoskeletal prote in expression could be that transplanted neurons undergo a new develop mental scheme (neodevelopment) that is brought about by truncated migr ation patterns and abnormal synaptic connections.