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| Behavior Analysis meets Biomedical Research: Advances in Interdisciplinary Research |
| Monday, May 25, 2015 |
| 4:00 PM–4:50 PM |
| 007B (CC) |
| Area: EAB; Domain: Basic Research |
| Chair: Maria Isabel Munoz Blanco (Universidad de Guadalajara) |
| CE Instructor: Christina M. Peters, M.Ed. |
| Abstract: Interdisciplinary study should be cooperative and reciprocal, in which neither of the disciplines is reducible to another or of less importance (Kantor, 1968). This aim is particularly challenging when understanding psychological events with respect to their biological correlates. Biomedical research is the broad area of science that looks for ways to prevent and treat diseases that cause illness and death in people and in animals (New Jersey Association for Biomedical Research, 2014). This area of study includes the understanding of diseases, the development of treatments, and techniques to reduce pain, all of which involve behavioral changes. An interdisciplinary collaboration between biomedicine and behavior analysis seems particularly relevant given behavior analysis’ characteristic refinement of tools and instruments for the measurement of behavioral change in both animals and humans. The present symposium presents several cases of interdisciplinary research, an animal model of autism, behavioral measurements of an animal surrogate for DMD, and an examination of behavioral impairments in a mouse model of Parkinson’s Disease, in which behavioral results complement biomedical research without compromising the integrity of both disciplines. |
| Keyword(s): Animal Research, Biomedical Models, Interdisciplinary Research |
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| The Effects of Inflammation on the Neuropathology of Autism |
| MARIA ISABEL MUNOZ BLANCO (Universidad de Guadalajara), Kenneth Hunter (University of Nevada School of Medicine), Linda J. Parrott Hayes (University of Nevada, Reno) |
| Abstract: A great deal of biomedical research has provided experimental evidence of the function of specific neuropeptides in the development of autistic symptomatology. There is evidence that individuals diagnosed with autism exhibit histological changes in the hippocampus (Bauman & Kemper, 1994; Bailey et al, 1998; Kemper & Bauman, 1998). Part of the research on neuropathology includes the study of inflammatory changes in the brain (Welch et al. 2005). The Maternal Immune Activation project (MIA) was created to investigate the notion that the neuropathology of autism is caused at least in part by the brain’s response to inflammation. This was accomplished by providing a behavioral account of the most characteristic symptoms of autism. Behavioral measurements were selected as a follow up from research on behavioral characteristics observed in children with autism (i.e. Bijou & Ghezzi, 1999; Spandin & Brady, 1999; Szabo, 2013), which included social deficits, learning and habituation deficits. The results of this research in which significant differences were found between experimental and control groups of mice will be presented. These results set the stage for a conversation on the importance of interdisciplinary research in this area as a means to provide a more comprehensive understanding of autism. |
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| A Behavior Analytic Assessment of “Cognitive" Deficits in a Mouse Model of Duchenne Muscular Dystrophy |
| CHRISTINA M. PETERS (University of Nevada, Reno), Matthew Lewon (University of Nevada, Reno), Linda J. Parrott Hayes (University of Nevada, Reno) |
| Abstract: In recent years, geneticists have engineered animal models for several diseases that commonly afflict humans. One of these models is known as the MDX mouse, a genetically modified mouse used in research as a surrogate for Duchenne muscular dystrophy (DMD). While the MDX mouse has been utilized effectively to research various cellular and muscular deficits associated with DMD, non-behavior analytic researchers have attempted to identify and study “cognitive" deficits of the MDX mouse with limited success. A careful review of the procedures utilized towards such ends reveals imprecise and misguided procedures to measure what researchers consider to be cognition. Utilizing a delayed non-matching to position (DNMTP) task and a conditioned suppression task, the authors of the present study seek to obtain more precise data regarding the overt behaviors of interest. Data from these efforts will be presented, and the issue of making the findings of the present study more “palatable" to an audience familiar with far less precise measures (e.g. T-maze, Object Recognition tests) will be discussed. The talk will conclude with a consideration of future directions for research and a commentary on the potential impact of this type of interdisciplinary research. |
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| Executive function deficits in a progressive MPTP mouse model of Parkinson's Disease |
| SUZANNE H. MITCHELL (Oregon Health & Science University), Katherine Stang (Oregon Health & Science University), Vanessa B. Wilson (Oregon Health & Science University), Lacy Pflibsen (Portland VA Medical Center), Michelle Sconce (Portland VA Medical Center), Charles Meshul (Oregon Health & Science University; Portland VA Medical Center) |
| Abstract: Behavioral alterations in Parkinson’s Disease (PD) are not limited to tremor and slowed movement. Increasingly cognitive impairment, including limited attentional processes, is recognized as a cardinal sign of the disorder. Further, reports suggest that these deficits can be experienced even in the early stages of the disorder. Research examining cognitive impairment from a behavior analytic standpoint is lacking, providing the focus for this research.
One widely-used model to progressively induce the loss of dopaminergic neurons characteristic of PD onset, involves administering mice a neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), over several weeks in increasing doses. To examine alterations in response to signals indicating the availability of positive reinforcement (attention), we developed a simple operant task in which mice responded in one of three nose-poke holes to earn a sucrose-solution reinforcer. The location of the criterion hole varied during the session but was signaled by a light above the manipulandum. Compared with animals receiving saline injections, performance on the task declined progressively as MPTP dose increased, despite mice exhibiting normal feeding patterns outside the operant environment. The hypothesis is explored that early-PD cognitive impairment may reflect the reduced ability to respond appropriately to discriminative stimuli and an increased avoidance of initiating potentially nonreinforced responses. |
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