Genecks Posted February 6, 2011 Posted February 6, 2011 (edited) I went to a talk about it yesterday (where a bunch of us scientists, multiple professors and students, were sitting around and someone presented it). It seemed pretty cool. It came out last month, though. A critical role for IGF-II in memory consolidation and enhancement http://www.nature.com/nature/journal/v469/n7331/full/nature09667.html We report that, in the rat, administering insulin-like growth factor II (IGF-II, also known as IGF2) significantly enhances memory retention and prevents forgetting. Inhibitory avoidance learning leads to an increase in hippocampal expression of IGF-II, which requires the transcription factor CCAAT enhancer binding protein β and is essential for memory consolidation. Furthermore, injections of recombinant IGF-II into the hippocampus after either training or memory retrieval significantly enhance memory retention and prevent forgetting. To be effective, IGF-II needs to be administered within a sensitive period of memory consolidation. IGF-II-dependent memory enhancement requires IGF-II receptors, new protein synthesis, the function of activity-regulated cytoskeletal-associated protein and glycogen-synthase kinase 3 (GSK3). Moreover, it correlates with a significant activation of synaptic GSK3β and increased expression of GluR1 (also known as GRIA1) α-amino-3-hydroxy-5-methyl-4-isoxasolepropionic acid receptor subunits. In hippocampal slices, IGF-II promotes IGF-II receptor-dependent, persistent long-term potentiation after weak synaptic stimulation. Thus, IGF-II may represent a novel target for cognitive enhancement therapies. From what I gather, injections of TGF-II help create a positive feedback loop that allows particular cells, those of which are involved in the retention and recall of memory, stay alive and generate even more TGF-II for themselves so they stick around. I could see some Flowers for Algernon (link) stuff being possible with this. Furthermore, the more interesting aspect, is that I doubt there would be a decrease in cell stability as would be found in the fictitious Flowers for Algernon book. The cells find a way to stabilize themselves. Questionable if a person could eventually develop a tolerance, as the chemical is extracellular and binds to receptors. Many drugs can pass through the cell or somehow interact with the phospholipid bilayer to affect what is inside of the cell. But this binds to a receptor outside of the cell. As it is independent of the cell machinery, TGF-II could help discover more aspects of what's inside the cell (neuron) via manipulation/application of TGF-II and seeing what new things form in neurons. Perhaps some correlations can be found with worms or invertebrates that have expansive nervous systems (ganglia) that reach into somatic regions. Edited February 6, 2011 by Genecks
CharonY Posted February 6, 2011 Posted February 6, 2011 I have not read the paper, however based on the description above it appears that synaptic plasticity appears to be affected (as e.g. by establishing persistent LTP or suchalikes) rather than cell viability. The latter of which would be, to my knowledge, rather unusual.
Genecks Posted February 6, 2011 Author Posted February 6, 2011 (edited) I have not read the paper, however based on the description above it appears that synaptic plasticity appears to be affected (as e.g. by establishing persistent LTP or suchalikes) rather than cell viability. The latter of which would be, to my knowledge, rather unusual. After taking a quick look at the article, I'd say there is definitely more ground to say synaptic plasticity is affected. I'd need more time to dissect the article. However, it seems as though it was implied that there was some cell viability and that a positive feedback loop was being created so that particular cells with applied TGF-II were sticking around. *reads a little harder once more* Thus, the IGF-IIdependentenhancement might not recruit the activation of new cells, but rather uses those that have been transcriptionally ‘marked’ by training and target synaptic mechanisms, possibly those at activated synapses. One of these mechanisms might be GSK3-regulated GluR1 synaptic mobilization, a hypothesis in line with previous reports of functional links between dendritic trafficking of GluR1 and GSK-3 (ref. 29), as well as between GluR1 and Arc expression, synaptic plasticity and memory consolidation25. We cannot exclude that IGF-II-dependent memory enhancement may occur via recruitment of new cell activation, which however would be independently from the activation and function of CREB-C/EBPb. Edited February 6, 2011 by Genecks
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