Furthermore, BrdU and Tunel experiments showed that the results were not a reflection of increased neuroblast proliferation prior to differentiation or differential apoptosis respectively as there were no differences between any of the experimental groups. The increased expression of Cx36 during development may provide enhanced cell-cell contact between neuronal progenitors and hence promote neuronal differentiation. A possibility supported by the dependence on Cx36 GJIC for neuronal coupling. Interestingly, the knockdown of Cx36 resulted in a decrease in the number of neurons and an increase in the number of GFAPpositive cells, which could suggest the decrease in neuronal differentiation, elicits a compensatory rise in astrocyte differentiation. The effects of Cx36 manipulation on neurogenesis were only observed in cells that had been expanded for 7 days or less suggesting that the cells have already become committed and no longer respond to Cx36 over expression or knock down. This suggestion fits with the observed decrease in endogenous Cx36 expression that occurs in NPCs after 14–21 days and with Cx36 transduction of 7 day old cultures having no effect on neuronal differentiation. To explore further the involvement of Cx36dependent gap junction communication in intra-neuronal communication and development experiments reflecting the in vivo composition of cells could be undertaken. This could be achieved using conditional Cx-36 transgenic mice and/or the stereotactic injection of viruses. Significantly following the lentiviral mediated overexpression of Cx36 in the intact hippocampus CA3 region of adult rats increased gamma oscillatory activity was measured. Results which further support Cx36 playing a significant physiological role in intra-neuronal gap junction communication in intact networks. In addition to the increase in the number of neurons following Cx36 over expression, we found the number of oligodendrocytes was also significantly increased. Oligodendrocytes are the myelinating cells of the CNS and act to insulate neuronal axons transmitting electrical impulses. It is also known that oligodendrocytes provide trophic factors that promote neuronal survival and hence there may be a cooperative SCH772984 relationship between neurons and oligodendrocytes during the differentiation process. The rise in oligodendrocytes observed may hence be due increased need for myelination and trophic factor support. Studies on transgenic mice lacking both Olig genes revealed that differentiation of motorneurons and oligodendrocytes was replaced with differentiation of interneurons and astrocytes. It may also be the case that an increase in the number of neurons provides a more supportive environment for the differentiation of oligodendrocytes and may explain.