Prior to joining NYMC, Eliana Scemes, Ph.D., held faculty positions at the University of Sao Paulo, Brazil, and later at Albert Einstein College of Medicine. Dr. Scemes has published 62 original studies, 13 review articles, 17 book chapters, and edited one book covering various medical specialties.

Education

• M.S., Zoology, Clinical Research Methods, Albert Einstein College of Medicine
• Ph.D., Physiology, Bioscience Institute, University of Sao Paulo, Brazil
• Postdoctoral in the Department of Neuroscience, Albert Einstein College of Medicine

Research

Dr. Scemes' laboratory investigates the role of gap junction proteins, specifically connexins and pannexins, in the pathophysiology of the nervous system. Using a range of animal models of central nervous system (CNS) disorders, her team studies the involvement of these proteins in conditions such as status epilepticus, experimental autoimmune encephalomyelitis (EAE), ischemia, neuroAIDS, and inflammatory pain. Their approach integrates a variety of techniques, including in vivo, in situ, and in vitro methods, as well as electrophysiology, immunohistochemistry, biochemistry, total internal reflection fluorescence, and calcium and confocal imaging.

Dr. Scemes' research centers on astrocyte-neuron communication, with a particular focus on the contributions of gap junctions and purinergic signaling to CNS disorders. Her current project examines the role of pannexin channels in astrocyte and neuronal ATP signaling and their implications for seizures.

Purinergic ATP-mediated signaling, a key mechanism by which astrocytes interact with neurons, is a major focus of her work. Non-lytic ATP release occurs through mechanisms such as pannexin1 (Panx1) channels, which are highly expressed in the CNS in both glial cells and neurons. Panx1 has been implicated in processes like ischemic neuronal death, neuroinflammation, and epileptiform activity. Her lab has shown that Panx1 channels mediate ATP release that exacerbates status epilepticus (SE). However, an unresolved question remains: whether astrocytes or neurons are the primary contributors to Panx1-mediated seizures.

The primary goals of her ongoing research are to determine the relative contributions of astrocytic and neuronal Panx1 channels to ATP release during status epilepticus and to elucidate the biophysical properties and signal transduction mechanisms underlying Panx1 channel activation in astrocytes and neurons.

To address these questions, her lab employs techniques such as field potential recordings from cortical-hippocampal slices of wild-type and transgenic mice, behavioral monitoring, and electroencephalographic (EEG) recordings of pharmacologically induced SE. To further investigate Panx1 activation, the lab conducts patch-clamp recordings from Panx1-null astrocytes and neurons expressing Panx1 mutants or peptides that target specific Panx1 domains critical for channel activation. These approaches aim to identify the molecular domains and signaling pathways involved in Panx1-mediated events.

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Publications

View All Publications

Professional Service

• Research Support Committee
• Ph.D. Admissions Committee
• Graduate Faculty Council
• Reviewer for Bridge and Seed Funding Grant Program TU

Teaching Responsibilities

• Neuroscience