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Aileen M. Bailey. Associate Professor of Psychology. B.A., Beloit College (1994); M.S., Ph.D., University of Georgia (1996, 1999)
I am interested in the neuroanatomy and neurochemistry of higher cognitive functions. In particular, I investigate the involvement of various neuroanatomical areas in a cognitively demanding task, learning set formation. Learning set formation is a task that is infrequently used by behavioral neuroscientists but offers a closer model to human learning than many of the heavily examined animal learning tasks. My laboratory has found that a general neurotoxin produces a profound impairment in the ability to form a learning set. However, a specific toxin that destroys only neurons that contain acetylcholine does not block learning set acquisition. My lab continues to investigate what areas of the brain are most crucial to this particular learning task. We will also be looking at pharmaceutical agents that might alleviate any impairment in learning set that we see following brain damage.
My lab has also begun investigating a mouse model of neurofibromatosis ( Nf1 ). Thirty to 60% of humans with Nf1 show some type of learning disability. We are currently characterizing the learning deficits in the Nf1 mouse working towards a way to alleviate any learning deficits seen.
Anne Marie Brady. Assistant Professor of Psychology. B.A., St. Mary's College of Maryland; M.A., Ph.D., Ohio State University (1997, 2000)
I am interested in the neurobiology of psychiatric diseases, particularly schizophrenia and drug addiction. I use animal models to study both the neuroanatomical and/or neurochemical dysfunctions and the behavioral and cognitive characteristics of these conditions. My current lines of research include:
(1) Investigation of cognitive deficits and neuroanatomical changes in a rat model of addiction called behavioral sensitization. Repeated administration of psychoactive drugs (e.g., amphetamines, cocaine) to rats results in changes in the brain that manifest as potentiated (sensitized) increases in drug-induced locomotor activity. Since many of the drug-induced alterations in neural circuitry involve areas that are heavily implicated in learning and memory, and human drug addicts often show cognitive impairments, I am interested in how these changes in the brain may translate into cognitive impairments in rats after repeated exposure to drugs. In this line of research, rats are given repeated doses of methamphetamine, are tested for behavioral sensitization, and are then tested in a battery of perceptual, motivational, and cognitive tasks. I am also interested in further characterizing the neuroanatomical changes that underlie behavioral sensitization using immunohistochemical staining for the expression of Fos, a protein encoded by an immediate early gene that is turned on when neurons are activated.
(2) Investigation of cognitive deficits in a rat model of schizophrenia. I use a rat model that is based on the neurodevelopmental theory of schizophrenia. Neonatal (7-day old) rats are given a specific lesion (brain damage) in the hippocampus, and are then allowed to grow to adulthood, when they begin to display behavioral and cognitive abnormalities that can be linked with common symptoms of schizophrenia (reduced social interactions, hyper-responsiveness to stress, hyper-responsiveness to dopaminergic drugs, impaired sensorimotor gating, impaired working memory). I am currently studying higher cognitive processes in these rats, including spatial learning and memory, attentional set-shifting, and formation of a learning set.
(3) Investigation of vulnerability to addictive behavior in two rat models of schizophrenia. Patients with schizophrenia are known to exhibit high rates of substance abuse, which may reflect increased vulnerability to addiction as a symptom of schizophrenia. I am studying the development of behavioral sensitization to methamphetamine in two animal models of schizophrenia - the neonatal lesion model described above, and the social isolation model in which animals are subjected to stressful rearing conditions during adolescence. I am also looking at neuroanatomical changes (Fos expression) following methamphetamine administration in both of these models.
Linda J. Coughlin. Associate Professor of Biology. B.S., Purdue University (1974), M.S., Medical University of South Carolina (1980), Ph.D., the George Washington University (1991)
My students and I focus on mu opiate receptors in the hypothalamus. Mu opiate receptors are the ones morphine binds to, although the natural neurotransmitters are endorphin, enkephalin and endomorphin. So the questions we ask are: What is the role of mu opiate receptors in the hypothalamus? I think the answer has to do with feeding behavior and energy expenditure. I am interested in how mu receptor activity might regulate other neuropeptides, such as leptin, melanocortin and neuropeptide Y, that also alter metabolism and body set point.
I also collaborate with Walter Hatch studying soft coral communication. My students and I study the pharmacology and molecular biology of the corals. Students discovered that the corals respond to nicotine, which mimics an alarm signal. They have also found that treating the corals with drugs that block nicotinic acetylcholine receptors can prevent alarm signaling with the "alarm substance". Currently we want to know if soft corals express an acetylcholine receptor.
I am also interested in how drugs of abuse change brain receptors and therefore behavior. I have most recently been working with a knockout mouse that is missing an adrenergic receptor. This mouse under-responds to amphetamine. We need to study the "behavioral phenotype" of this knockout mouse for additional clues to how adrenergic receptors might work in normal animals.
Eric J. Hiris. Associate Professor of Psychology. B.A., Oakland University (1990); M.S., Ph.D., Vanderbilt University (1992, 1995)
My research focuses on visual perception, specifically how people perceive moving objects and complex patterns of motion. The properties of neurons in the visual areas of the brain are well known, but how do those neurons give rise to the experience of seeing that we have? How can knowledge of the properties of neurons be used to understand how the system as a whole works? What sort of non-invasive studies of humans can shed light on how we see? Current projects include:
1) Biological motion--If observers are shown motion displays consisting of points of light attached to the joints of a moving human, observers can readily identify the human form and the activity being performed. I am interested in several aspects of biological motion.
a) How well can observers determine the sex of the actor in such displays? How do stereotypes about sex-appropriate activities influence such sex judgments?
b) How do additional moving dots mask the perception of biological motion displays? What are the critical temporal and spatial factors?
c) Although biological motion is thought by many to be a relatively pure 'motion' stimulus, it is clear that information about form and structure play a role in perceiving biological motion. How important is this role?
2) Motion-induced blindness--If observers view a large field of motion with several conspicuous but stationary objects, these stationary objects disappear from awareness. This stunning illusion can be used to understand how the brain selects visual information for further processing.
Wesley P. Jordan. Professor of Psychology. BS, University of Puget Sound (1974); Ph.D., Dartmouth College (1979).
As a behavioral neuroscientist, I am interested in how the brain controls behavior. In particular, I want to know how the brain is changed as a result of learning and how memories are stored. Most of my work involves studying how rats (and their brains) learn in simple situations in the laboratory. Specific areas of active research include the brain mechanisms supporting habituation, a simple form of learning to disregard unimportant stimuli; cocaine sensitization, a process by which repeated low doses of cocaine produce a heightened sensitivity to subsequent doses of this drug; and animal models of psychopathology.
Pamela S. Mertz. Assistant Professor of Chemistry. B.A., Juniata College (1992); Ph.D., Mayo Graduate School (1999)
My current research involves studying insulin-signaling pathways in pre-adipocytes. Efforts are focused on how certain divalent metal ions such as chromium and vanadium affect different processes inside the cell. I also have broader research interests in the area of enzymology, in particular studying phosphatases and metalloenzymes. In the past I have worked with calcineurin, a phosphatase that is abundant in brain and is involved in various signaling pathways. Functions in the brain include involvement with memory, long-term potentiation, and regulation of many types of ion channels.
John Ramcharitar. Assistant Professor of Biology. B.S., The University of the West Indies (1991); M.Phil., The University of the West Indies (1997); Ph.D., University of Maryland, College Park (2003)
In my laboratory, we investigate structure-function relationships in fish auditory systems. Fishes are by far the most abundant vertebrates on the planet (>24,000 species!!!), and they show phenomenal diversity in hearing capabilities. Much of this diversity correlates with an equally impressive array of auditory structures. Additionally, fishes show tremendous variations in the ability to process acoustic stimuli, and in the ability to extract biologically significant sounds from “noisy” environments. Given the increase in human-generated sound in many of the local waterways and systems, studies of fish hearing may be especially important for assessing the effects of anthropogenic noise on aquatic animals. We use anatomical (e.g. scanning electron microscopy) and electrophysiological (e.g. auditory evoked potentials) techniques to explore the fascinating world of fish auditory biology.