Bradley Roberts

Education & Training 

I completed my BA in Neuroscience & Biology at St. Mary's College of Maryland in 2015. During my time at St. Mary's as an undergraduate researcher, I worked with Prof. Aileen Bailey investigating the role of orexin in the basal forebrain on cortical-dependant executive functions (Piantadosi et al. (2015), Brian Research), and with Prof. Samantha Elliott investigating the effects of Vitamin C as a novel anti-cancer therapeutic (Roberts et al. (2015), BIOS). I also completed a research placement at the Armed Forces Research Institute of Medical Sciences (AFRIMS) with Dr. Eric Lombardini investigating the pathology of male breast cancer in primate models (Roberts et al. (2014), Journal of Medical Primatology). 

For my undergraduate thesis research project, I collaborated with Prof. Brian Mathur at the University of Maryland School of Medicine. My dissertation focused on targeting striatal fast-spiking interneurons in a mouse model of Parkinson's disease using an in vivo optogenetic approach. After graduating, I returned to Brian's lab as a Research Assistant (2015-2016), where I investigated the role of striatal fast-spiking interneurons in encoding action velocity dynamics using miniature endoscopic in vivo calcium imaging technologies, as well as collecting tract tracing immunohistological and patch-clamp electrophysiology data to assist other ongoing projects (Patton et al. (2016), Neuropsychopharmacology; White et al. (2018), Cell Reports; Cover et al. (2019), Cell Reports; Patton et al. (2019), Neuropsychopharmacology).

DPhil Thesis research

I joined the Laboratory of Monoamine Transmission led by Prof. Stephanie Cragg in the Department of Physiology, Anatomy & Genetics in October 2016. During my DPhil, I have investigated the influence the chief inhibitory neurotransmitter, GABA, has on dopamine output in mammalian striatum, using electrophysiology and fast-scan cyclic voltammetry technologies. Initial work revealed that dopamine release in striatum is under tonic inhibition by a local ambient GABA tone, which critically limits striatal dopamine output through direct action at GABA_A and GABA_B receptors (Lopes*, Roberts* et al. (2019), Journal of Neuroscience). 

More recently, I have been investigating how local striatal GABA sources may be altered in Parkinson's disease and therefore have implications on both dopamine release and striatal output. To do this, I am using a prodromal genetic mouse model which overexpresses human α-synuclein at disease relevant levels, developed here at the Oxford Parkinson's Disease Centre (OPDC). 

In the Autumn of 2019, I will begin a Junior Research Fellowship with St. John's College, Oxford.