Research Areas

Forecasts of Stress Resilience

On both preclinical and clinical levels, not all individuals express depressive symptoms in response to stressful experiences. Traditionally, animal models examining stress responsivity employ prior manipulation or an additional, possibly stressful procedure to observe stress-induced changes in performance. We are currently examining the use of ultrasonic vocalizations as a novel indicator of stress resilience. Our work has demonstrated rats that emit 22-kHz vocalizations during an intermittent cold-water swim stress are behaviorally resilient to subsequent stress. Presently, we are validating the use of 22-kHz as “alarm calls” or “safety-signals” to conspecifics as a method of active coping. The ability to predict behaviorally how an individual will react to stressors is beneficial to our understanding of stress resiliency. Measures of immobility, or lack of active coping, have been used as an endpoint to determine stress-induced behavioral depression. We are also currently examining how activity or lack of activity during stress induction can predict resilience or vulnerability in conjunction with ultrasonic vocalizations.

Comorbidity of Anxiety and Depression

Our lab is expressing a growing interest in a variety of depression called "anxious depression," which as the name suggests, refers to the experience of simultaneously suffering from symptoms of both anxiety and depression. This particular combination is correlated with difficulty in coping, a poorer rate of recovery, and more severe symptoms of depression. Although depression and anxiety disorders may appear to be one in the same, they are in fact separate (albeit, often related) disorders. Depression can be described as a person experiencing lethargy, despair, and a sense of hopelessness. On the other hand, an anxiety disorder (e.g., obsessive-compulsive disorder or post-traumatic stress disorder) is identified by patients expressing fear, panic, and nagging worry.  The confusion that often accompanies these disorders may stem from their treatments, as the same antidepressants and behavioral therapies provide some relief for those experiencing either of these disorders.  We find some similarities between our swim stress model and the shock stress model through certain anxiety measures, suggesting our paradigm may be a novel model for post-traumatic stress disorder.  It is our hope that investigating this variation of depression (i.e., anxious depression) will help to lead to more effective and appropriate treatments for depressed patients.

Controllability and Learning and Memory

Exposure to inescapable stress has been shown to interfere with subsequent learning and memory. We have developed a stress controllability paradigm using forced swimming as the stressor. We have tested the effects of stress and coping in this paradigm on standard shuttle-escape learning as well as navigational learning and memory in the Morris water maze task. We find fundamental differences between our model and the standard shock stress controllability paradigm. We are currently exploring the noradrenergic correlates involved in aversively motivated forced swimming behaviors and water-maze spatial learning.


It is clear that stress can alter both the endocrine and immune systems. These systems are critical for our ability to effectively fight off disease. In addition, the nature of stress as well as the ability to cope with stress affects these two systems. We are interested in endocrine and immune endpoints including corticosterone and cytokine production following inescapable stress exposure. We find some similarities and some differences between our swim stress model and the standard shock stress model. Currently these quantifiable endocrine and immune correlates of stress resilience are being investigated in animals emitting 22-kHz ultrasonic vocalizations.

Stress Controllability and Drug Reactivity

Our research examines the influence of swim stress on the behavioral reactivity to antidepressant compounds. We have found differences between our model and the standard shock model to sensitivity to certain antidepressants during the forced swim test procedure. Furthermore, we are investigating the potentiation of swim stress induced ultrasonic vocalizations by antidepressant administration thereby predicting resilience or vulnerability. Moreover, we are interested in the central nervous system sites of action of minor tranquilizers, and understanding how emotion or stress can alter the effects of these compounds. Using shock, swim, and restraint stress, and a rotarod treadmill for measuring motor incoordination, we have shown that the nature of the stress and stress controllability markedly influence the ataxic potency of these compounds. We plan on complementing the above findings with analysis of the endogenous ligands of the benzodiazepine/GABA receptor in the future as a correlate of stress resilience.


University of New Hampshire
Robert Drugan's Lab