Hartman Behavioral Neuroscience Lab


Rich E. Hartman

Professor of Psychology

School of Behavioral Health

Loma Linda University


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CV / Publications

I am a professor of experimental psychology and direct the Behavioral Neuroscience Lab at Loma Linda University in southern California. I graduated from Missouri State University in 1993 with a BS in experimental psychology. I then enrolled in the Behavior, Brain & Cognition program at Washington University in St. Louis, where I studied rodent behavior and neurodegeneration under behavioral expert Dave Wozniak in John Olney's lab. During this time, I helped Dave set up Washington University's Animal Behavior Core facility. I defended my PhD dissertation on September 11, 2001, and then trained for 4 years as a postdoc in the lab of Alzheimer's disease guru Dave Holtzman. While in the Holtzman lab, I worked with a number of transgenic and knockout mouse models of Alzheimer's disease and learned biochemical/histological techniques for assessing biomarkers of neuropathology. I have been publishing papers characterizing rodent behavioral phenotypes since 2001. My first paper characterizing neuropathology following brain injury used a mouse model of traumatic brain injury. Since then, I have published papers characterizing brain injury resulting from early drug exposure, global ischemia, intracerebral hemorrhage, and impact trauma, as well as characterizing a number of transgenic mouse lines and neuroprotective strategies.

Our behavioral neuroscience lab at Loma Linda University in southern California primarily uses animal models of neurological disease to understand their mechanisms and potential therapeutic treatments. Techniques used include behavioral assessment (e.g., water maze) of rats and genetically modified (transgenic / knockout) mice, pharmacology (e.g., manipulation of behavior with various drugs), small animal surgery (e.g., intracardial perfusion, induction of ischemic stroke and/or traumatic brain injury), histology / immunohistochemistry (e.g., visualization of neurons and  Alzheimer’s-like amyloid plaques in brain slices), stereological microscopy (unbiased quantification of brain structures under a microscope), and biochemistry (e.g., protein assays of brain tissue using Western blot and ELISA).

Long-standing collaborations with other labs here (John Zhang, Jiping Tang, Andy Obenaus, Bill Pearce, Denise Bellinger, Larry Longo, and Steve Ashwal) have yielded several publications characterizing rodent models of juvenile and adult brain injury (e.g. traumatic brain injury, stroke, radiation) and treatments for these injuries (monoclonal antibody, pomegranate, stem cells, melatonin, osteopontin, fingomilod, MMP inhibition, DJNK inhibition, hemodilution, and aquaporin-4 RNA interference). Our lab also functions as the Neurobehavioral Core Facility for Loma Linda University’s Hemorrhagic Stroke Center. The lab’s main interests lie in exploring the interface between acute brain injury (e.g., TBI, stroke, radiation) and subsequent neurodegeneration (e.g., Alzheimer’s neuropathology) and in dissecting the mechanisms by which plant-based compounds (phytochemicals) can influence the brain’s functions under these conditions.

We have shown that traumatic brain injury can accelerate the development of Alzheimer’s-like neuropathology in transgenic mice  (Hartman et al., 2002) and rats (Pop et al., 2012), and that preventing accumulation of amyloid plaques in their brains with a monoclonal antibody (Hartman et al., 2005) or pomegranate phytochemicals (Hartman et al., 2006) can prevent the age-related decline in cognition seen in these animals. Interestingly, pomegranate supplementation reduced soluble amyloid-β and plaques by ~50% in the brains of transgenic mice. More importantly, we showed that dietary supplementation with pomegranates improved learning and memory performance in the mice  and in humans after heart surgery (Ropacki et al 2013). Other experimental data from our lab demonstrates that pomegranate supplementation protected against depression-like behaviors (learned helplessness) induced by radiation exposure (Dulcich & Hartman 2012) and improved swim speed in transgenic mice. Presumably, these effects are mediated by phytochemicals like polyphenols (including the phenolic acids and flavonoids), which have been shown to have antioxidant properties and to suppress inflammatory and other pathways.

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