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Darrin Brager, Ph.D., is an Assistant Professor in Cell and Molecular Neuroscience within the Biology faculty of the School of Life Sciences at the University of Nevada, Las Vegas (UNLV). He directs the Brager Cellular Neurophysiology Lab and participates in the Interdisciplinary Graduate Program in Neuroscience. Brager received his Bachelor’s degree in Zoology from the University of Florida, Master’s degree in Biological Sciences from Florida Atlantic University, and Ph.D. in Physiology from the University of Maryland School of Medicine in Baltimore. He conducted postdoctoral research at Baylor College of Medicine in Houston before joining the faculty at the University of Texas at Austin, where he remained for 18 years prior to relocating his laboratory to UNLV.
The Brager Lab examines the cellular and molecular mechanisms of brain function, focusing on voltage-gated ion channels to link pathological neuronal activity with behavioral phenotypes in rodent models of neurological disorders such as Fragile X syndrome, temporal lobe epilepsy, depression, and tuberous sclerosis. Research employs electrophysiological methods including whole-cell somatic and dendritic patch clamp recordings, cell-attached and outside-out patch clamp recordings, synaptic physiology and plasticity studies, acute brain slice preparations, electrical and optogenetic stimulation, Ca²⁺ imaging, and supporting biochemical and histological techniques to explore deficits in neurotransmitter release, ligand-gated channels, voltage-gated channels, and dendritic disorders. Key publications encompass “Activity-dependent regulation of intrinsic excitability in hippocampal CA1 pyramidal neurons” (Fan et al., Nature Neuroscience, 2005), “Plasticity of intrinsic excitability during long-term depression is mediated through mGluR-dependent changes in Ih in hippocampal CA1 pyramidal neurons” (Brager and Johnston, Journal of Neuroscience, 2007), “Impaired dendritic expression and plasticity of h-channels in the fmr1−/y mouse model of Fragile X syndrome” (Brager et al., Cell Reports, 2012), “Cell-type specific channelopathies in the prefrontal cortex of the fmr1−/y mouse model of Fragile X syndrome” (Kalmbach et al., eNeuro, 2015), “Perisomatic changes in h-channels regulate depressive behaviors following chronic unpredictable stress” (Kim et al., Molecular Psychiatry, 2017), and “Reduced dendritic Na+ current impairs dendritic spike generation in L5 PFC neurons in a mouse model of Fragile X syndrome” (Brandalise et al., Journal of Physiology, 2023).

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