Research Interests
My research interests focus on adaptive neural processes in brain as reflected in molecular and behavioral indices following chronic exposure to alcohol, stress, and/or cytokines and other select pharmacological agents. A primary current focus is to employ a repeated ethanol exposure and withdrawal paradigm in rodent models to examine the contribution of different neurotransmitter systems to the progressive worsening of alcohol withdrawal (e.g., sensitization or “kindling’ of anxiety-like behavior) that is unique to cycled, as opposed to continuous, ethanol exposure and withdrawal. We have found that selective repeated stress exposures interact with future chronic ethanol exposure to increase anxiety-like behavior and to render animals vulnerable to future stress or ethanol. We have also found that pharmacological agents for corticotrophin releasing factor, benzodiazepine, or 5-HT2C receptors can strongly influence this sensitization process as do select cytokines. Comparable studies with adolescent rats are examining the impact of cycled stress, withdrawal, and select pharmacological treatments on this sensitization process. Collaborative efforts with Dr. Todd Thiele in the Psychology Department are focused on the interactions of peptide systems, including NPY and the melanocortin system in alcohol preference and related behaviors.
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Recent Publications
Click here for a full list of publications from PubMed
Sparta DR, Fee JR, Knapp DJ, Breese GR, Thiele TE. (2007). Elevated anxiety-like behavior following ethanol exposure in mutant mice lacking neuropeptide Y (NPY). Drug Alcohol Depend. 2007 May 3; [Epub ahead of print]
Breese GR, Knapp DJ, Overstreet DH, Navarro M, Wills TA, Angel RA (in press). Repeated lipopolysaccharide (LPS) or cytokine treatments sensitize ethanol withdrawal-induced anxiety-like behavior. Neuropsychopharmacology
Knapp DJ, Overstreet DH, Breese GR (2007). Baclofen blocks expression and sensitization of anxiety-like behavior in an animal model of repeated stress and ethanol withdrawal. Alcohol Clin Exp Res 31(4):582-595.
Qin L, Wu X, Block ML, Liu Y, Breese GR, Hong JS, Knapp DJ, Crews FT (2007). Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration. Glia 55(5):453-462.
Ferraro III FM, Sparta DR, Knapp DJ, Breese GR, Thiele TE (2006). Increased consumption but not operant self-administration of ethanol in mice lacking the RIIβ subunit of protein kinase A (PKA). Alcohol Clin Exp Res 30(5):825-35.
Fee JR, Knapp DJ, Sparta DR, Breese GR, Picker MJ, Thiele TE (2006). Involvement of protein kinase A in Ethanol-induced locomotor activity and sensitization. Neuroscience 140:21-31.
Overstreet, DH, Knapp DJ, Angel RA, Breese GR (2006). Reduction in repeated ethanol withdrawal-induced anxiety-like behavior by site-selective injections of 5-HT1A and 5-HT2C ligands. Psychopharmacology 187(1):1-12.
Breese GR, Knapp DJ, Criswell, HE, Moy, SS, Papadeas, ST, Blake BL (2005). The Neonate-6-hydroxydopamine-lesioned rat: A model for clinical neuroscience and neurobiological principles. Brain Res Rev. 48(1):57-73.
Knapp DJ, Overstreet DH, Breese GR (2005) Modulation of ethanol withdrawal-induced anxiety-like behavior during later withdrawals by treatment of early withdrawals with benzodiazepine/gamma-aminobutyric acid ligands. Alcohol Clin Exp Res 29(4, April):553-63.
Breese GR, Overstreet, DH, Knapp, DJ (2005). Conceptual framework for the etiology of alcoholism: a “kindling”/stress hypothesis. Psychopharmacology 178(4):367-380.
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Bowles Center for Alcohol Studies at the University of North Carolina at Chapel Hill