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Postbac Seminar Series: January 19, 2023

Series: Science Skills; Speaking

Jan 19, 2023

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:

Braden Oldham, NIA

Title: Dopaminergic modulation in the Lateral Entorhinal Cortex: Implications in Parkinson’s Disease and dementia.

Abstract: Ventral Tegmental Area (VTA) dopaminergic neuron (DAN) degeneration is present in Parkinson’s, Alzheimer’s Disease, and other forms of dementias. Multiple genetic mouse models reflect memory deficits, specifically episodic memory components encoded by the VTA efferent, Lateral Entorhinal Cortex. To understand and elucidate dementia related therapeutic targets, we investigate the neurotransmitter, cell, and circuit functions of VTA to LEC DAN’s in episodic memory. To evaluate, I genetically modulated both pre- and post-synaptic DA transmission revealing a decrease of temporal precision in fear and reward-based episodic learning tasks.

Bio: Braden is in his final months as a Post-bacc in Huaibin Cai’s Systems Neuroscience Lab at the NIA. He graduated from Creighton University with a BS in Neuroscience and BA in Classical and Near Eastern Studies. He will be entering an MD/PhD program in the fall where he hopes to continue using the Systems techniques and knowledge gained to uncover functional correlates and functional therapies for neurologic and psychiatric diseases and disorders.


Lauryn Ridley, NIAID

Title: Using molecular modeling and biochemical analysis to examine the effect of the sickle cell mutation on the interactions between hemoglobin and eNOS

Abstract: Patients with severe malaria have decreased bioavailability of the vasodilator nitric oxide and impaired endothelium-dependent vasoregulation. In animal models of severe malaria, treatment with nitric oxide reverses endothelial dysfunction and improves survival. In human arteries, nitric oxide signaling is regulated by biophysical interactions between endothelial nitric oxide synthase (eNOS) and hemoglobin (Hb), but the precise nature of these interactions remains elusive. To better understand the interactions between eNOS and Hb, we applied structural modeling and molecular dynamics simulation (MDS) to predict critical interfaces between these two proteins. Our goal is to assess the impact of amino acid substitutions in the beta globin chain, such as the sickle cell mutation (HbS), on the binding affinity between Hb and eNOS. This knowledge could lead to new therapeutic approaches to modulate endothelial nitric oxide signaling.

Bio: In 2022, Lauryn Ridley graduated from St. Mary’s College of Maryland with a B.S. in Biochemistry and Biology and a minor in Neuroscience. In undergrad she conducted research in Dr. Pamela Mertz’s lab, where she worked on the expression and purification of recombinant avian corticosterone-binding globulin as part of a broader study of zebra finch stress physiology. Currently, Lauryn is a fellow in NIAID’s Physiology Unit at the Laboratory of Malaria and Vector Research led by Hans Ackerman. The Physiology Unit studies the role of endothelial globins as regulators of nitric oxide signaling and the impact of human globin gene variants on vascular function and disease risk. Lauryn is a member of NIAID’s Intraumural Research Opportunities (INRO) Program, and aspires to become a physician who conducts biomedical and public health research, ultimately to provide care for under-resourced communities.


Samra Beyene, NICHD

Title: Anterior Versus Posterior Bias in CGE-Derived Interneuron Subtypes

Abstract: One of the fundamental questions of developmental neuroscience is how do neurons acquire specialized molecular, morphological, and physiological fates in the mammalian forebrain? The subpallium (or ventral telencephalon) gives rise to ɣ-aminobutyric acid-containing (GABAergic) cell types, such as long-range inhibitory projection neurons and inhibitory cortical interneurons. Based on morphology and gene expression profiles, the subpallium can then be further divided into germinal zones called the medial, caudal, and lateral ganglionic eminences (MGE, CGE, and LGE respectively). The MGE, CGE, and LGE also differ in  the types of interneurons they give rise to in the mature brain. Notably, the MGE gives rise to PV and SST cortical interneurons, and the CGE gives rise to VIP, Reelin (non-SST), and CCK cortical interneurons. Within the MGE, microdissection and transplantation techniques performed over 15 years ago linked cell fate with distinct spatial domains: SST cells preferentially arise from the dorsal MGE whereas PV cells arise from the ventral MGE. However, similar experiments have never been performed for the CGE. Leveraging a similar cell transplantation assay, we aim to characterize the spatial origin of distinct CGE-derived interneuron subtypes.

Bio: Samra graduated from Brown University in the spring of 2022 with an honors degree in Biochemistry and Molecular Biology. While at Brown, Samra was a member of Erica Larschan’s lab where she studied FMRP, a protein that when mutated leads to a common heritable neurodevelopmental disorder called Fragile X Syndrome. Upon matriculation, Samra joined Dr. Timothy Petros’s lab in NICHD as a Post-baccalaureate IRTA fellow and Developing Talents Scholar. She has enjoyed learning a host of new cellular and molecular techniques, and looks forward to using these skills in future studies at the intersection of genetics and neurodevelopment.