With the time window coincidence, training-protocol dependence, and the disruption with the amn mutant and subsequent rescue of both behavioral memory and cellular memory trace, the strength of evidence tying the DPM memory trace to ITM is very strong. The evidence is also very strong for the argument that the γ MB neuron trace is

relevant to late-phase LTM. Time window coincidence, training-protocol dependence, and bumping the system in two different ways —reducing CREB and CaMKII activity—alters both memory trace and long-term behavioral memory in parallel. The conclusion that the LTM trace of the α/β MBNs is fundamental to long-term behavioral memory is inescapable. Time window coincidence, training-protocol dependence, and 30 disruptions that alter the memory trace and this website long-term behavioral memory in parallel tie these together and elevate this trace

to arguably the most convincing memory trace relevant to behavior discovered in any organism to date. The other extreme to the model presented above is that perhaps each node forms traces representing all temporal forms of behavioral memory, such that each node would have at least one trace representing STM, ITM, and LTM. This requires that all of check details the neurons have the capability of forming multiple temporal forms of memory, but there are precedents for this. Aplysia sensory neurons are capable of forming short-term, intermediate-term, and long-term facilitation in response to the application of serotonin, although the mode of induction determines which types of plasticity will emerge ( Stough et al., 2006 and Puthanveettil and Kandel, 2011). Similarly, different temporal forms of synaptic plasticity are evident in the hippocampus depending on the type of

stimulation used to produce the plasticity ( Roberson et al., 1996 and Sacktor, 2008). Of course, the ability of individual Methisazone neurons to form different temporal forms of synaptic plasticity does not necessarily mean that this expansive role will be adopted when in the context of the brain of a behaving animal. Do the memory traces described above drive behavior over the window of time of their existence? This critical question, of course, is extremely difficult to answer with current technology. It would be necessary to implant the memory trace in some artificial way and then determine whether the organism exhibited behavioral memory. Although progress has been made in activating neural circuits used for memory formation using optogenetic approaches (Schroll et al., 2006 and Claridge-Chang et al., 2009), the advances made to date have been limited to activating circuitry representing the reinforcer rather than the sensory information that is learned, which may be represented in a more complex way by the nervous system. It is likely that an understanding of the mechanisms by which the memory traces are generated will be needed before approaching the aforementioned question.