Dayan Knox
Dayan Knox
Office location
University of Delaware, 105 The Green, Room 217, Wolf Hall, Newark, DE 19716
Lab
Delaware Biotechnology Institute, 15 Innovation Way, Newark, DE
Education
- Ph.D. – The Ohio State University
- M.A. – The Ohio State University
- B.S. – North Carolina Central University
Biography
Dayan Knox, Ph.D., is an associate professor in the Department of Psychological and Brain Sciences at the University of Delaware. Originally from Trinidad and Tobago, Knox completed his undergraduate schooling at North Carolina Central University; master's and Ph.D. training at The Ohio State University; and postdoctoral study at the University of Michigan Medical School.
His research interests concern stress and learning and memory. Peripheral hormones and central ascending arousal systems contribute to emotional learning and memory. These systems are also sensitive to stress, and under certain circumstances, may contribute to emotional memory processes that contribute to psychiatric disorders (e.g. PTSD, substance abuse). Knox explores how stress-induced changes in peripheral hormonal, ascending arousal, and emotional circuit systems contribute to stress-induced effects that model specific symptoms in psychiatric disorders.
Courses Regularly Taught
PSYC314: Brain and Behavior
NSCI320: Intro to Neuroscience
NSCI629: Integrative Neuroscience
Research Projects
Area: Behavioral Neuroscience
Current definitions of the extinction circuit in the mammalian brain focus on medial prefrontal cortical inhibition of amygdala activity and subcortical substrates. We have previously shown that cholinergic neurons in the medial septum and diagonal bands of Broca (MS/DBB) are critical for acquisition of extinction. However, neural circuitry through which these neurons modulate extinction memory processes are unknown. In this study, we test the hypothesis that MS/DBB cholinergic input to the dorsal hippocampus is critical for acquisition of extinction memory.
We have previously shown that exposing rats to single prolonged stress results in extinction retention deficits. However, it is not clear if this is due to enhanced fear memory or deficits in extinction memory. Our previous attempts to address this question using behavioral methods were inconclusive. In this study we used changes in expression of transcription factors as measures of neural activity to map neural activity throughout the fear circuit during fear memory formation and extinction memory formation. By doing this we will attempt to determine if single prolonged stress exposure leads to extinction retention deficits by altering neural activity during fear memory formation or extinction memory formation.
We have previously shown that exposing rats to single prolonged stress results in extinction retention deficits and that inhibiting glucocorticoid release during fear conditioning exacerbates these deficits. These previous findings suggest that single prolonged stress-induced changes in glucocorticoid receptors can be adaptive. We will test this hypothesis by showing that activation of glucocorticoid receptors in the ventral hippocampus of single prolonged stressed rats during fear conditioning leads to attenuated extinction retention deficits in rats exposed to single prolonged stress.
