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Postbac Seminar Series: September 20, 2022

Series: Science Skills; Speaking

Sep 20, 2022

This event is recommended for: Postbacs.

Science isn't complete until the results have been shared with others, and talking about your results is one of the important ways of making them public. The Postbac Seminar Series provides a unique opportunity for two Postbacs each month to present their research to a diverse audience of their peers.  The atmosphere is relatively informal and non-threatening.  The series allows Postbacs who attend to learn about the different types of biomedical research being conducted at the NIH while meeting other postbacs.  Read more about the seminar series.


The meeting information will be shared by email. If you have questions, please contact Runa Cheng <> and Marc Theberge <>.


This month's presenters are:

Jordan Meza, NIAAA

Title: Increasing neuronal activity within the medial temporal lobe rescues spatial learning and memory deficits in the Scn2a mouse model of autism.

Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder caused by genetic and/or environmental insults. In humans, haploinsufficiency of the SCN2A gene, which encodes the voltage gated sodium channel Nav1.2, is strongly associated with ASD and often co-presents with intellectual disability (ID). Typically, ID manifests as deficits in learning ability, episodic memory (recalling personal experiences) and spatial memory. Greater understanding of the circuits and cellular processes underlying this disorder will aid in novel ASD treatment development. A deficit in learning and memory was confirmed in Scn2a+/- mice by using a Barnes Maze spatial learning task where mice navigate a 20-hole maze to locate a single escape hole. Additionally, cFos+ neurons were imaged and quantified in whole brains of Scn2a+/-; Fos-EGFP mice to identify regions where basal neuronal activity is abnormal. There were significantly reduced numbers of cFos+NeuN+ neurons in six brain regions, four of which are reciprocally connected and functionally linked with memory impairments in humans, rodents, and primates. Because these 4 regions are cortical, I chose to conditionally delete Scn2a in cortical excitatory pyramidal (PYR) neurons, which replicated the spatial learning deficit. Furthermore, recovery of spatial learning ability was achieved by chemogenetically increasing dendritic depolarization levels in the same population of cortical PYR neurons, suggesting reduced depolarization in these principal neurons contribute to Scn2a-associated spatial learning impairments. This research identifies brain regions that may be pharmacologically targeted to relieve ID in individuals with SCN2A haploinsufficiency.

Bio: Jordan Meza graduated from Vanderbilt University in 2021 with a major in Neuroscience. During undergraduate, he worked as a research assistant in Dr. Eugenia Gurevich’s pharmacology lab studying the effect of psychostimulants on GPCR function. Currently, he works in the NIAAA’s Section for Neural Circuits under Dr. Michelle Antoine researching the neural localization and cellular mechanisms underlying genetic ASD variants. He is particularly interested in how systems in the brain work together to enable complex cognitive abilities.


Sandeep David , NIDCD 

Title: Kif1aa-based transport along microtubules maintains synaptic vesicle populations in hair cells

Abstract: Sensory hair cells utilize specialized ribbon synapses to reliably transmit sensory information to the brain. Ribbon synapses have high rates of spontaneous vesicle release and function without fatigue. To sustain this level of release, a continuous supply of synaptic vesicles must be trafficked to the presynapse. In neurons, the motor protein Kif1a has been shown to transport synaptic vesicles along microtubules to the presynapse. Whether Kinesin-mediated transport delivers synaptic vesicles along microtubules to the hair cell presynapses is not known. Using zebrafish as our model, we are able to examine the effects of the loss of Kif1aa in hair cells in vivo and find that Kif1aa is required to localize synaptic vesicles at the presynapse.

Bio: Sandeep graduated from the University of Maryland in May 2021 with a degree in Physiology & Neurobiology, and he joined Dr. Katie Kindt’s lab in the Section on Sensory Cell Development and Function in the NIDCD in July 2021. In his free time, Sandeep enjoys playing soccer and disc golf, the latter of which he unceasingly tries to get his friends into. He intends to pursue a PhD in neuroscience with the hope of continuing his research studying sensory hair cells.


Audrey Phan, NINDS

Title: Memory Retrieval Reinstatement of Neural Connectivity Patterns 

Abstract: Successful memory retrieval has been shown to occur with reinstatement of neural activity first present during encoding. Previous evidence has shown memory reinstatement of oscillatory power at the level of individual electrodes; however, it is unknown whether groups of electrodes reinstate their network connectivity patterns during memory retrieval. We examined this question using intracranial electroencephalography data captured from 20 participants with medically refractory epilepsy as they performed a paired-associates verbal memory task. We first identified connected electrode pairs in the temporal lobe by selecting pairs of electrodes in this region that exhibited strong correlations with a consistent time lag across random segments of recording data. We next calculated the connectivity of these pairs at the maximal time lag while participants were performing the paired-associates verbal memory task. We calculated the similarity of connectivity patterns across electrode pairs in the temporal lobe between encoding and retrieval periods. Our data revealed a significantly higher encoding-retrieval similarity in the observed connectivity patterns for correct retrieval trials as compared to incorrect retrieval trials. Collectively, these results suggest that successful memory retrieval entails the reinstatement of regional network connectivity patterns initially present during memory encoding.

Bio: Audrey Phan graduated from UC Berkeley in 2021 with Highest Honors in Cognitive Science. At Berkeley, she conducted research in the D’Esposito Cognitive Neuroscience Lab investigating the neural mechanisms of cognitive control using neuroimaging and transcranial magnetic stimulation. She is currently a postbac at NINDS in the Functional Neurosurgery Section, where she studies the neural mechanisms underlying memory using human intracranial electroencephalography data. Audrey is currently applying to MD/PhD programs and hopes to improve neuropsychiatric medicine as a future physician-scientist. In her free time, she loves to read, practice yoga, and make art.