While the molecular and cellular mechanisms underlying the acquisition, consolidation, reconsolidation and retrieval of memory have attracted a considerable amount of attention in neuroscience, very little is known about memory allocation, the process that determines which neurons in a network store a given memory. Computationally, it is highly advantageous to be able to correctly "file" and "cross-reference" memories in the brain, and memory allocation provides for this. Previous results from our laboratory have suggested that the transcription factor CREB (cAMP-response element binding protein) has a role in memory allocation; increasing the level of CREB in a subset of neurons increased the probability that these neurons stored a memory. Initially, I explored the functionality of these CREB-biased memory neurons by specifically activating them, utilizing a novel technique called optogenetics. I demonstrated that activation of only the CREB-biased memory neurons is sufficient to elicit recall. This confirms a widely held, yet hitherto largely unproven, belief in the neuroscience community that activating the specific neurons that store a memory will lead to the retrieval of that memory. Although mechanisms for CREB's role in memory allocation have been proposed, to date, none has been validated. Here, I have established that increasing neuronal excitability (the likelihood that a neuron responds to a given input) in a subset of neurons can allocate memories in a way analogous to increasing levels of CREB. These results are highly suggestive that increased neuronal excitability is the mechanism by which CREB allocates memory. This research will advance not only our understanding of CREB's role in memory allocation, it will also elucidate memory mechanisms that could ultimately aid in the development of treatments for disorders thought to be caused by abnormal memory allocation, including post-traumatic stress disorder (PTSD).