We have provided the most direct evidence showing a cause-effect relation between synaptic plasticity and memory formation (Nabavi et al., 2014, Nature). With the use of optogenetics fortified by in vitro/in vivo recording and behavioral assays we generated an associative memory and showed that we could repeatedly turn off and on this associative memory simply by changing synaptic strength (inducing LTD and LTP).
An immediate question following this study is how these newly formed memories are integrated into the existing network. This is a vital concern for any system that aims to store and retrieve information. Our brain is continuously exposed to external sensory inputs. This amount of information can overwhelm any storage device no matter how large its capacity. Therefore, a challenge for our brain is to decide which information is worthy of permanent storage. The storage process itself, however, poses another challenge: how to integrate new information into a network of pre-existing memories without “catastrophic interference” (forgetting).
The first challenge is commonly known as synaptic consolidation, which takes place within the first minutes to hours after memory formation. The second challenge, known as systems consolidation, is a slower process that takes weeks, months or even years. The major focus of my research is to understand how our brain tackles these challenges. To this end we will use a combination of tools such as molecular biology, in vitro and in vivo electrophysiology, two-photon laser scanning microscopy, optogenetics, behavioral analysis (i.e. whatever it takes) to move forward.
These studies may lead us to better understand and treat neuropsychological diseases thought to be related to aberrations in synaptic plasticity, such as posttraumatic stress disorder, schizophrenia, substance abuse disorders and dementia.