Association for Behavior Analysis International

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.

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.