Memory manipulation has become one of the most hotly pursued topics in neuroscience. After all, much or of who are is based on what we’ve learned, including memories that we can consciously recall as well as acquired desires and habits that can lead to problems like addiction. In rodents, we’ve known for decades that damage to the hippocampus can erase recently-formed memories. Studies of reconsolidation have shown us that when a memory is retrieved it becomes labile and allows for new information to be added, thereby creating an updated version. More recently we (humans) have been able to identify the neurons involved in memory formation and show that killing them, and only them, results in memory erasure. Bringing us even closer to the stuff of movies, studies by Garner et al. in Science and Liu et al. in Nature have now artificially controlled memory formation and recall. We’re essentially talking about reactivating memory by pushing a button. Yes – you can say “dude, whoah” now. Continue reading Forming and recalling memories. Artificially.
Previously, I wrote about new SFN data on the role for newborn neurons in regulating emotion. The second half of the SFN meeting rounded out the story because the bulk of the functional presentations focussed on the role of new neurons in that other, classic function of the hippocampus: memory. Spanning synaptic plasticity, circuit function, and then linking it all to behavior, we have quite a complete story here.
SYNAPTIC PLASTICITY IN YOUNG NEURONS
Every time I get worked up about all various neurogenesis findings I think about one acronym that returns me to a state of inner peace: ACSF-LTP. Yes, I plagiarized that last line from my previous post. We all know about LTP right? The ability of synapses to strengthen their connections in response to activity? It has been used for decades as a physiological model of memory formation. It’s pretty well accepted that newborn neuron ACSF-LTP is a unique form of LTP – one that is insensitive to GABAergic inhibition (hence “Artificial Cerebro Spinal Fluid” LTP, in contrast to LTP that also requires inhibition of GABA neurotransmission), one that requires a the NR2B subunit of the NMDA receptor, and one that is induced more easily than that of mature neurons. ACSF-LTP has quite a history: Continue reading Saving the best for last: neurogenesis, plasticity and memory. #SFN11