|Modeling Prefrontal Cortex-Related Behavioral Dysfunction After Developmental and Adult Neural Insults
|Monday, May 30, 2016
|5:00 PM–5:50 PM
|Zurich C, Swissotel
|Area: BPN/EAB; Domain: Basic Research
|Chair: Cole Vonder Haar (University of British Columbia)
|Discussant: Megan R. Heinicke (California State University, Sacramento)
Animal models of diseases and disorders are essential for the development of effective treatments and therapies. However, the degree of behavioral assessment is frequently limited in animal models, despite relevance to the human condition. This symposium will highlight current uses of operant behavioral techniques in the assessment of central nervous system damage. Specifically, it will focus on fields that have historically relied on very basic assessments of sensorimotor functioning or even eschewed behavioral outcome measures in favor of markers of neural damage and dysfunction. A presentation from Dr. Kris Martens will cover the assessment of choice impulsivity following experimental traumatic brain injury, and a presentation from Dr. Chris Newland will describe functional assessments after developmental exposure to toxicants. Finally, Dr. Megan Heinicke will discuss the implications of these animal models for developing therapeutics. Together, these studies suggest that operant techniques offer numerous advantages for modeling human-relevant dysfunction in a variety of animal models. Further development of these procedures could lead to vastly improved detection therapeutic efficacy and increase the likelihood of translation to humans.
|Keyword(s): Injury, neuroscience, rat, translational
Choice Impulsivity Is Increased After Experimental Traumatic Brain Injury Regardless of Severity
|KRIS M. MARTENS (University of British Columbia), Cole Vonder Haar (University of British Columbia)
Traumatic brain injury (TBI) affects 2.5 million Americans each year, leading to the development of long-term deficits in function. Impulsivity is one of the major problems reported following brain injury in humans. Despite the scope of this problem, few animal studies have addressed chronic behavioral deficits and studies of impulsivity are nearly nonexistent. Recent research in our laboratory using a frontal model of brain injury in rats has demonstrated considerable increases in motor impulsivity. In the current work, we evaluated choice impulsivity using the delay discounting procedure and assessed the effects of TBI. Following either a mild or severe brain injury, rats demonstrated a reduced tolerance for delay that continued for the duration of the eight weeks of testing. This data suggests that brain injury, independent of the severity can lead to chronic changes in impulsivity. Behavioral models of these types of deficits could be key to understanding the TBI-related pathophysiology resulting in chronic dysfunction and help devise therapeutics to alleviate it.
|Experimental Models of Environmental Contaminants: Analysis, Understanding, and Treatment
|M. CHRISTOPHER NEWLAND (Auburn University)
|Abstract: Our understanding of how environmental contaminants act relies heavily on experimental laboratory models, which are important because they reveal the mechanisms by which contaminants disrupt behavior and how one might intervene to prevent or even reverse such damage. Operant techniques are especially important because they model voluntary behavior, which is what we are frequently concerned about. Laboratory models reveal what contaminants do. Drawing from our research of methylmercury exposure, I will describe how this contaminant affects cognitive and motor function and how we have addressed questions about prevention or amelioration of damage. We have also tested the functional relevance of hypotheses about neurobiological mechanisms of action using operant behavior. This research has not just yielded an appreciation of a contaminant but, more broadly, about how events that disrupt early cortical development can have subtle, long-lasting effects on operant (voluntary) behavior.