Recent efforts on immune-neural interaction center on the effects of cytokines on neurons as well as glial cells. We have found that tumor necrosis factor-a (TNF-a), a cytokine implicated in autoimmune demyelinating disorders, causes cell processes to retract, and inhibits K+ currents in OLGs. Interestingly, none of the aforementioned effects of TNF-a applies to sympathetic neurons. Instead, incubation of sympathetic neurons with TNF-a leads to an increase in Ca2+ current and nicotinic receptor current density. 

Ongoing research is directed at understanding the mechanisms of action of the putative messengers involved in TNF-a signaling, i.e. arachidonic acid or its metabolites, and sphingomyelin hydrolysis products. We hypothesize that crosstalk among different lipid-derived second messengers may play an important role in determining the ultimate outcome in response to TNF-a or other cytokines. An approach combining biochemical, electrophysiology, fluorescence imaging, and selected molecular biology techniques will be employed in these studies. We are also looking at the expression of TNF receptors in brain slices under normal and pathological conditions using a combination of immunohistochemistry and in-situ hybridization. 

Lastly, we have started working in the area of glial repair and regeneration, specifically on signaling mediated by growth factors. The information derived from this research is likely to have important implications for autoimmune neuralgic disorders (e.g. multiple sclerosis, CNS AIDS), spinal cord/brain injury as well as provide insight into the regenerative capacity of neural cells. 

 Attali B, Wang N, Kolot A, Sobko A, Cherepanov V and Soliven B. (1997) Characterization of delayed rectifier KV channels in oligodendrocytes and progenitor cells. J. Neurosci, 17:8234-8245.