Presentation Title
The Role of Melanocortins and Prevention of Cognitive Deficits in an Early Life Seizure Model
Abstract
Early Life Seizures (ELS) are often associated with subsequent cognitive deficits that are detrimental to quality of life. Frequently these deficits present themselves within the realm of executive function and similar psychological comorbidities such as ADHD. Recent work in our lab has demonstrated improved cognitive ability in a rat model of ELS upon administration of the endogenous melanocortin Adrenocorticotropic Hormone (ACTH) when compared to a vehicle control. In addition, ACTH induced benefits above and beyond those of Dexamethasone, a common corticosteroid. This suggests that ACTH acts to prevent cognitive deficits in a manner separate from a corticosteroidal anti-inflammatory response. Despite these marked benefits, the specific mechanism of action remains uncertain. Here, we begin to identify the means of action taken by ACTH in prevention of ELS-mediated cognitive deficits. Techniques such as seizure inductions, cognitive behavioral testing, and immunohistochemistry were implemented for this purpose. ELS mice treated with ACTH exhibited improved performance on a fear-extinction task compared to their untreated ELS counterparts, confirming the prior results found in rats. Effects of ACTH treatment on a specific strain of transgenic mouse, seizure presentation, and brain cell populations are currently under investigation and the findings will be discussed.
Primary Faculty Mentor Name
Amanda Hernan
Status
Undergraduate
Student College
College of Arts and Sciences
Program/Major
Neuroscience
Primary Research Category
Biological Sciences
The Role of Melanocortins and Prevention of Cognitive Deficits in an Early Life Seizure Model
Early Life Seizures (ELS) are often associated with subsequent cognitive deficits that are detrimental to quality of life. Frequently these deficits present themselves within the realm of executive function and similar psychological comorbidities such as ADHD. Recent work in our lab has demonstrated improved cognitive ability in a rat model of ELS upon administration of the endogenous melanocortin Adrenocorticotropic Hormone (ACTH) when compared to a vehicle control. In addition, ACTH induced benefits above and beyond those of Dexamethasone, a common corticosteroid. This suggests that ACTH acts to prevent cognitive deficits in a manner separate from a corticosteroidal anti-inflammatory response. Despite these marked benefits, the specific mechanism of action remains uncertain. Here, we begin to identify the means of action taken by ACTH in prevention of ELS-mediated cognitive deficits. Techniques such as seizure inductions, cognitive behavioral testing, and immunohistochemistry were implemented for this purpose. ELS mice treated with ACTH exhibited improved performance on a fear-extinction task compared to their untreated ELS counterparts, confirming the prior results found in rats. Effects of ACTH treatment on a specific strain of transgenic mouse, seizure presentation, and brain cell populations are currently under investigation and the findings will be discussed.