Understanding how cell assemblies code for memory encoding and recall

We are interested in determining how neurons in the hippocampus and its sub-regions can code and recall memory events. Why do the neural circuits in the subiculum have such a distinct role than other hippocampal areas? These investigations are done using calcium imaging, electrophysiology and optogenetics in freely behaving mice performing cognitive tasks.

What is the neural mechanism of memory consolidation during sleep?

The hippocampus and other brain regions play important role in enhancing the conversion of memory to long-term memory during sleep. However, there are at least two different states in sleep; slow-wave and rapid-eye movement (REM)-sleep. How do these two sleep states contribute to memory consolidation? We are interested in identifying the mechanisms underlying these two states in memory consolidation.

Investigating the role of  the septum in memory

The septum is divided into the medial and the lateral septum. The medial septum provides a powerful input to the hippocampus and entorhinal cortex and has been shown to play a critical role in memory-related hippocampal oscillations while the lateral part receives a massive input from the hippocampus, and provide a circuit important for the association between spatial contextual cues and reward. We are interested in understanding how the different cell types of the medial and lateral septum contribute to memory encoding and recall in freely behaving mice.

Developing new methods to visualize and manipulate memory- related  neurons  during behaviour.

There is a revolution going on in neuroscience concerning the recent developments of research tools for observing and manipulating neurons during cognition. My laboratory as invested a great deal of efforts to develop the latest methods of optogenetics, electrophysiology, and, more recently, calcium imaging of neuronal populations using miniature microscopes in freely behaving mice.

How circuits are altered in Alzheimer’s disease and finding approaches to reverse memory deficits in AD.

While there is ample evidence of how individual neurons are affected in AD, we poorly understand how neuronal dynamics at the population level are affected. One important goal we have is to use optogenetics to re-establish normal population dynamics and memory function in AD mice models.