Staff Directory

My previous work studied the mechanisms underlying the regulation of dendritic oxytocin release and the characterization of central oxytocinergic signaling pathways. To pursue my interests, I used multiple techniques including electrophysiological methods (whole-cell patch-clamp, calcium imaging, and optogenetics), quantitative fluorescent microscopy (epifluorescence and two-photon), and immunohistochemistry. My current research interests at Columbia lie in the delineation of the functions of hippocampal ventral CA2 from the aspects of both cellular physiology and system functions. 

We are interested in the molecular and cellular mechanisms underlying electrical signaling and synaptic transmission in the nervous system, and how these electrical signals give rise to complex behaviors. We focus on how ion channels and synaptic transmission regulate information flow in the cortico-hippocampal circuit, which plays a critical role in learning and memory. One area of research explores the role of the hyperpolarization-activated cation channels (the HCN channels) in regulating dendritic integration of excitatory and inhibitory synaptic inputs. We found that genetic deletion of the HCN1 channel from hippocampus enhances synaptic excitation, the induction of long-term plasticity and, surprisingly, spatial learning and memory. As these channels have also been implicated in various neurological and psychiatric diseases, we are now examining the molecular mechanisms that regulate HCN1 channel expression and trafficking in both normal and disease states. A second project examines the role of the CA2 subregion of the hippocampus, an area first identified in 1934 but which has received little attention over the past 80 years. We have developed a mouse like that enables us to selectively inactivate CA2, which we find produces a very specific deficit in the encoding of social memory, the ability of an animal to recognize and remember a conspecific. We are now examining the CA2 neural circuitry in more detail to determine how this region participates in memory encoding. As data from individuals with schizophrenia and autism spectrum disorders suggest the presence of alterations in the CA2 region, we are using mouse models of neuropsychiatric disease to explore the possible role of altered CA2 function in the social endophenotypes of these disorders.

_{(photo credit: John Abbott)}

My research is focused on characterizing the neural circuit mechanisms and activity patterns of the hippocampus underlying memory of salient experiences which inform adaptive behaviors. 

With a strong background in computational neurosciences acquired during my training at ETH Zurich, I combine experimental and analytical work in the Siegelbaum lab to assess the cortico-hippocampal circuit mechanisms of adaptive social behaviors. Specifically, I am interested in the memory-related mechanisms and computations underlying the encoding and recall of aversive social experiences. Based on a 'social memory hypothesis' of social fear, I investigate how disruption of such mechanisms can lead to generalized social avoidance, as observed in neuropsychiatric disorders such as social anxiety, autism spectrum disorder, or schizophrenia. My research relies on a multidisciplinary approach where I use social fear and social memory assays, manipulation and monitoring of genetically defined cell populations and projections and computational analysis and modelling of social and other variables.

Github: https://github.com/PegahKa

My research focuses on understanding how emotional valence is integrated into social memory circuits to guide behavior. During my doctoral work at UMC Utrecht, I investigated how distinct neuronal ensembles in the ventral tegmental area represent positive and negative emotional states. At Columbia, I am extending this approach with a particular interest in how neurons represent the identity of others and how these representations acquire emotional meaning through experience. By examining how these neuronal ensembles form, change, and influence behavior, I aim to elucidate the circuit principles that support social memory and how their disruption may contribute to disorders of social cognition.

I assist in administration and administer assistance.

I am a molecular biologist by training, and my research at Columbia has mostly focused on studying the role of a particular class of voltage-gated ion channels in the brain: the HCN pacemaker channels. I’ve used proteomics to identify regulatory partners for these channels in different parts of the brain, which are important for determining their expression, properties and subcellular distribution. More recently, I generated humanized mouse models that reproduce mutations in HCN1 associated with severe forms of childhood epilepsy. I work in collaboration with in vivo and in vitro electrophysiologists to understand how seizures develop in these mice, and how they can best be treated.