Eric Krause

Eric Krause Ph.D.

Associate Professor & Director, Center for Integrative Cardiovascular & Metabolic Diseases

Department: SR-VP FOR RESEARCH
Business Phone: (352) 273-6977
Business Email: ekrause@cop.ufl.edu

Research Profile

Stress, broadly defined as a real or perceived threat to homeostasis, activates neural circuits that alter the body’s physiology and behavior to ensure survival and well-being. The Krause Lab employs the rodent model to investigate how the central nervous system coordinates behavioral and physiological responses to stress. In particular, the lab studies how signals associated with dehydration impact the central pathways regulating stress responding and mood.

For example, loss of body fluids increases circulating levels of angiotensin II (ANGII), which activates the angiotensin type-1 receptors (AT1R) in various tissues to increase fluid intake, promote water and electrolyte retention and elevate blood pressure. Interestingly, the same neural circuits that regulate the influence of ANGII on hydromineral balance and cardiovascular function are also recruited during responding to psychological stress. Our studies have demonstrated that ANGII targets the brain via activation of AT1R in the subfornical organ (SFO), a specialized nucleus with an incomplete blood-brain-barrier, to coordinate the endocrine, cardiovascular and behavioral limbs of the stress response. These observations have led us to hypothesize that the AT1R in the SFO may be the site of convergence for the co-morbidity of psychopathology and cardiovascular disease.

In contrast to loss of body fluids, increasing plasma sodium concentration (pNa) elicits thirst by activating osmoreceptors in the brain. Acute increases in pNa suppress circulating ANGII and greatly elevate oxytocin levels centrally and systemically. Given that ANGII stimulates stress-responding and oxytocin is documented to have anti-stress properties especially when the stressor that is employed is social in nature, we predicted that acute osmotic dehydration would attenuate stress-responsiveness. Indeed, our studies have found that rats systemically administered a concentrated NaCl solution have decreased endocrine and cardiovascular responses to psychological stress exposure. Additionally, rats given NaCl engaged in more interactions when presented with unfamiliar conspecifics, suggesting that acute salt-loading decreases social anxiety. These observations have led to the hypothesis that acute increases in pNa attenuate stress-responsiveness, which may promote the social interactions that are encountered when engaging in drinking behavior. We are currently using this model to provide insight towards mechanisms underlying psychopathologies accompanied by cardiovascular irregularities like social phobias, anxiety and panic disorders.

My research utilizes an integrative approach towards investigating brain circuits governing physiology and behavior. We use chronic stress paradigms (i.e. visual burrow system or chronic variable stress) to model psychiatric disorders in rodents. Tract tracing, immunohistochemistry and in situ hybridization are used to characterize the neuroanatomical circuits mediating stress responding. Subsequently, we administer lentiviral vectors into brain nuclei that compose the circuit to inhibit the expression of targeted genes and reveal their contribution to stress responding and mood. To evaluate the limbs of the stress response, hormonal, cardiovascular and behavioral outcomes are assessed. Recently, we’ve obtained the angiotensin receptor flox mouse and plan to employ the cre-lox system to inhibit the expression of this receptor in select tissues.

Grants

March 2019ACTIVE
Crosstalk between dopamine and glucocorticoids in high levels of nicotine intake and anhedonia in rats
NATL INST OF HLTH NIDA ·
January 2019ACTIVE
Interrogating distinct angiotensin type-1 and type-2 receptor containing brain circuits to understand and alleviate hypertension
NATL INST OF HLTH NHLBI · Project Manager
July 2018ACTIVE
Ethanol dysregulation of oxytocin-mediated reward
NATL INST OF HLTH NIAAA ·
December 2017ACTIVE
Neurons expressing angiotensin type 2 receptors in the NTS as an access point for cardiovascular control.
NATL INST OF HLTH NHLBI · Principal Investigator
December 2017ACTIVE
Targeting brain angiotensin signaling to discern and alleviate stress-related disease.
NATL INST OF HLTH NHLBI · Principal Investigator
August 2016ACTIVE
OR-DRPD-ROF2016: A Neurodevelopmental Theory of Social and Environmental Isolation in Autism
UF OFFICE OF RESEARCH ·
June 2016 – February 2019
Optogenetic control of neuronal pathways that mediate re
NATL INST OF HLTH NIMH ·
April 2016ACTIVE
Brain-Gut Microbiome-Immune Axis in Hypertension
NATL INST OF HLTH NHLBI · Project Manager
December 2014ACTIVE
Central Mechanisms Underlying the Stress Dampening Effects of Acute Hypernatremia
NATL INST OF HLTH NHLBI · Principal Investigator
July 2013 – May 2019
Angiotensin and neuroimmune activation in hypertension
NATL INST OF HLTH NHLBI · Project Manager

Education

2005
Ph.D.
Florida State University
2002
M.S.
Florida State University
1999
B.A.
Hiram College