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Dive into the research topics where A. Courtney DeVries is active.

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Featured researches published by A. Courtney DeVries.


Behavioral Neuroscience | 1999

The effects of oxytocin and vasopressin on partner preferences in male and female prairie voles (Microtus ochrogaster).

Mary M. Cho; A. Courtney DeVries; Jessie R. Williams; C. Sue Carter

This study compared the effects of centrally administered oxytocin (OT) and arginine vasopressin (AVP) on partner preference formation and social contact in male and female prairie voles (Microtus ochrogaster). After 1 hr of cohabitation and pretreatment with either AVP or OT, both males and females exhibited increased social contact and significant preference for the familiar partner. After pretreatment with either an OT receptor antagonist (OTA) or an AVP (V1a) receptor antagonist (AVPA), neither OT nor AVP induced a partner preference. In addition, treatment with OT+OTA or AVP+AVPA was associated with low levels of social contact in both sexes. Either AVP or OT is sufficient to facilitate social contact if either the OT or AVP receptor is available. However, the formation of partner preferences may require access to both AVP and OT receptors.


Physiology & Behavior | 2003

Social modulation of stress responses.

A. Courtney DeVries; Erica R. Glasper; Courtney E. Detillion

Social interactions can profoundly affect the hypothalamic-pituitary-adrenal (HPA) axis. Although most research on social modulation of glucocorticoid concentrations has focused on the consequences of exposure to stressful social stimuli, there is a growing body of literature which suggests that social support in humans and affiliative behaviors in some animals can provide a buffer against stress and have a positive impact on measures of health and well-being. This review will compare HPA axis activity among individuals for whom social relationships are maintained through aggressive displays, such as dominance hierarchies, vs. individuals engaging in high levels of prosocial behavior. We also will examine oxytocin, a neuropeptide that is well known for promoting social behavior, as the physiological link between positive social interactions and suppression of the HPA axis. Despite many examples of social interaction modulating the HPA axis and improving health outcomes, there is relatively little known regarding the underlying mechanisms through which social behavior can provide a buffer against stress-related disease.


Experimental Neurology | 2004

Chronic behavioral testing after focal ischemia in the mouse: functional recovery and the effects of gender

Xiaoling Li; Kathleen K. Blizzard; Zhiyuan Zeng; A. Courtney DeVries; Patricia D. Hurn; Louise D. McCullough

Several useful behavioral tests exist for measuring behavioral recovery after ischemia in higher-order animals and rats. With the increasing use of mice in focal stroke research, simple, reliable, and reproducible behavioral testing has become a priority. As neuroprotective agents are tested, long-term outcome must be assessed, especially in studies focused on neuronal plasticity and regeneration after ischemia. Our laboratory and others have previously shown that estrogen (E2) is neuroprotective in rodent stroke paradigms. We examined a battery of behavioral tests in male and female mice subjected to 90 min of middle cerebral artery occlusion (MCAO) to determine the most sensitive tests for detecting sensorimotor dysfunction after stroke, and to determine the functional significance of E2-mediated neuroprotection. Only two tests, the corner test and the cylinder test, were able to differentiate between groups (sham and stroke) after several days of repeated testing. The cylinder test was sensitive to the neuroprotective/neurorestorative effects of E2, but 2 weeks after stroke, the cylinder test was unable to distinguish between sham and stroke animals treated with E2. In contrast, the corner test was able to differentiate stroke and sham animals even 6 weeks after stroke, but did not distinguish animals treated with E2 vs. vehicle. These tests provide a simple, rapid, reliable assessment of sensorimotor dysfunction in the mouse after focal ischemia. Hormonal status influences speed of recovery on cylinder testing in animals of both genders. This suggests that a short battery of tests including the neurological score, cylinder, and corner test may be adequate to rapidly and repeatedly assess sensorimotor dysfunction in mice of both genders.


Psychoneuroendocrinology | 2004

Social facilitation of wound healing

Courtney E. Detillion; Tara K.S. Craft; Erica R. Glasper; Brian J. Prendergast; A. Courtney DeVries

It is well documented that psychological stress impairs wound healing in humans and rodents. However, most research effort into influences on wound healing has focused on factors that compromise, rather than promote, healing. In the present study, we determined if positive social interaction, which influences hypothalamic-pituitary-adrenal (HPA) axis activity in social rodents, promotes wound healing. Siberian hamsters received a cutaneous wound and then were exposed to immobilization stress. Stress increased cortisol concentrations and impaired wound healing in isolated, but not socially housed, hamsters. Removal of endogenous cortisol via adrenalectomy eliminated the effects of stress on wound healing in isolated hamsters. Treatment of isolated hamsters with oxytocin (OT), a hormone released during social contact and associated with social bonding, also blocked stress-induced increases in cortisol concentrations and facilitated wound healing. In contrast, treating socially housed hamsters with an OT antagonist delayed wound healing. Taken together, these data suggest that social interactions buffer against stress and promote wound healing through a mechanism that involves OT-induced suppression of the HPA axis. The data imply that social isolation impairs wound healing, whereas OT treatment may ameliorate some effects of social isolation on health.


Stroke | 2005

Neuroprotective Properties of the Natural Vitamin E α-Tocotrienol

Savita Khanna; Sashwati Roy; Andrew Slivka; Tara K.S. Craft; Soma Chaki; Cameron Rink; Margaret A. Notestine; A. Courtney DeVries; Narasimham L. Parinandi; Chandan K. Sen

Background and Purpose— The current work is based on our previous finding that in neuronal cells, nmol/L concentrations of &agr;-tocotrienol (TCT), but not &agr;-tocopherol (TCP), blocked glutamate-induced death by suppressing early activation of c-Src kinase and 12-lipoxygenase. Methods— The single neuron microinjection technique was used to compare the neuroprotective effects of TCT with that of the more widely known TCP. Stroke-dependent brain tissue damage was studied in 12-Lox-deficient mice and spontaneously hypertensive rats orally supplemented with TCT. Results— Subattomole quantity of TCT, but not TCP, protected neurons from glutamate challenge. Pharmacological as well as genetic approaches revealed that 12-Lox is rapidly tyrosine phosphorylated in the glutamate-challenged neuron and that this phosphorylation is catalyzed by c-Src. 12-Lox-deficient mice were more resistant to stroke-induced brain injury than their wild-type controls. Oral supplementation of TCT to spontaneously hypertensive rats led to increased TCT levels in the brain. TCT-supplemented rats showed more protection against stroke-induced injury compared with matched controls. Such protection was associated with lower c-Src activation and 12-Lox phosphorylation at the stroke site. Conclusion— The natural vitamin E, TCT, acts on key molecular checkpoints to protect against glutamate- and stroke-induced neurodegeneration.


Stroke | 2000

Cognitive Deficits After Focal Cerebral Ischemia in Mice

Kimihiko Hattori; Hanna Lee; Patricia D. Hurn; Barbara J. Crain; Richard J. Traystman; A. Courtney DeVries

BACKGROUND AND PURPOSE The interpretation of cognitive data in many experimental stroke studies is problematic because middle cerebral artery occlusion (MCAO) is associated with sensorimotor alterations that may become confounding factors in cognitive testing. The purpose of the current study was to determine if it is possible to measure MCAO-induced cognitive deficits by using short durations of ischemia that do not result in alterations in sensorimotor behavior in mice. METHODS Male C57/Bl6 mice were subjected to 60 or 90 minutes of intraluminal MCAO or sham surgery. In the first cohort of animals (n=12/group), locomotor activity, balance, and coordination were evaluated 2 weeks after surgery. In a second cohort of animals (n=10/group), the effects of 60 minutes of MCAO on subsequent learning and memory were assessed with a step-down passive avoidance task beginning 1 week after surgery. In a third cohort of animals (n=8 to 10/group), training in a passive avoidance task was completed before 60 minutes of MCAO, then retention of the task was assessed 1 week after surgery. In all animals, infarction size was determined after 14 days of reperfusion with use of cresyl violet staining and quantitative image analysis. RESULTS There was no significant difference in infarction volume in the cerebral cortex or caudoputamen after 60 versus 90 minutes of MCAO. However, there was a significant increase in latency to move 1 body length in the 90-minute MCAO group compared with the 60-minute MCAO and sham groups. In 2 additional cohorts of animals, 60-minute MCAO was associated with a deficit in the acquisition and retention of a passive avoidance task regardless of whether the task training occurred before or after MCAO. CONCLUSIONS Long-term cognitive deficits can be induced in mice by using a short duration of MCAO (60 minutes) that does not result in concomitant sensorimotor deficits.


Proceedings of the National Academy of Sciences of the United States of America | 2001

Social stress exacerbates stroke outcome by suppressing Bcl-2 expression

A. Courtney DeVries; Hung Dong Joh; Ora Bernard; Kimihiko Hattori; Patricia D. Hurn; Richard J. Traystman; Nabil J. Alkayed

The relationship between stressful life events and the onset of disease is well documented. However, the role of psychological stress as a risk factor for life-threatening cerebrovascular insults such as stroke remains unspecified, but could explain individual variation in stroke outcome. To discover the mechanisms through which psychological stress may alter stroke outcome, we modeled the effects of chronic social intimidation and stress on ischemia-induced bcl-2 expression and early neuronal cell loss resulting from cerebral artery occlusion in mice (C57BL/6). The bcl-2 protooncogene promotes cell survival and protects against apoptosis and cellular necrosis in numerous neurodegenerative disorders, including stroke. In our study, male mice were chronically exposed to aggressive social stimuli before induction of a controlled, mild ischemic insult. Stressed mice expressed ≈70% less bcl-2 mRNA than unstressed mice after ischemia. In addition, social stress greatly exacerbated infarct in wild-type mice but not in transgenic mice that constitutively express increased neuronal bcl-2. Despite similar postischemic concentrations of corticosterone, the major stress hormone in mice, high corticosterone concentrations were significantly correlated with larger infarcts in wild-type mice but not bcl-2 transgenic mice. Thus, enhanced bcl-2 expression offsets the potentially deleterious consequences of high postischemic plasma corticosterone concentrations. Taken together, these data demonstrate that stressful prestroke social milieu strongly compromises an endogenous molecular mechanism of neuroprotection in injured brain and offer a new behavioral target for stroke therapy.


Neuroscience & Biobehavioral Reviews | 2001

Cognitive and behavioral assessment in experimental stroke research: will it prove useful?

A. Courtney DeVries; Randy J. Nelson; Richard J. Traystman; Patricia D. Hurn

Stroke in humans is associated with deficits in sensorimotor and cognitive function. Consequently, many stroke researchers recently have expanded their techniques to assess cognitive and behavioral correlates of histologically-determined stroke damage in animal models. Although the incorporation of functional outcome assessment represents an important step forward in stroke research, reports of middle cerebral artery occlusion (MCAO) induced behavioral deficits often conflict, and a significant correlation between post-stroke histology and behavior has been reported in few stroke studies. Discrepancies in behavioral outcomes among studies may be due to several factors, such as method of MCAO, duration of occlusion, strain, the timing and method of the behavioral testing and the laboratory environment. Furthermore, proper experimental and control groups, necessary to rule out potential confounding factors during cognitive testing, often are not incorporated. The goal of this review is: (1) to provide a description of the techniques most commonly employed to assess functional outcome after (MCAO) in rodents and (2) to identify potential confounding factors that may interfere with a clear interpretation of the behavioral data.


Biological Psychology | 2011

Oxytocin increases autonomic cardiac control: Moderation by loneliness

Greg J. Norman; John T. Cacioppo; John S. Morris; William B. Malarkey; Gary G. Berntson; A. Courtney DeVries

The current study examined the role of perceived social isolation in moderating the effects of oxytocin on cardiac autonomic control in humans. Intranasal administration of 20 IU oxytocin resulted in a significant increase in autonomic (parasympathetic and sympathetic) cardiac control. Specifically, oxytocin increased high frequency heart rate variability, a relatively pure measure of parasympathetic cardiac control, and decreased pre-ejection period, a well-validated marker of enhanced sympathetic cardiac control. Derived metrics of autonomic co-activity and reciprocity revealed that oxytocin significantly increased overall autonomic cardiac control. Furthermore, the effects of oxytocin on cardiac autonomic control were significantly associated with loneliness ratings. Higher levels of loneliness were associated with diminished parasympathetic cardiac reactivity to intranasal oxytocin. The effects of OT on autonomic cardiac control were independent of any effects on circulating pro-inflammatory cytokine or stress hormone levels. Thus, lonely individuals may be less responsive to the salubrious effects of oxytocin on cardiovascular responsivity.


Journal of Neuroendocrinology | 2003

Reduced Aggressive Behaviour in Mice with Targeted Disruption of the Oxytocin Gene

A. Courtney DeVries; W. Scott Young; Randy J. Nelson

Oxytocin (OT) has been reported to mediate aggressive and affiliative behaviours in several species. The behavioural role of OT has been established with physiological manipulations that potentially affected blood pressure, which may have indirectly affected the behaviours under study. To provide converging evidence of the physiological role of OT in aggressive behavior, wild type (WT), heterozygous (OT−/+), and homozygous (OT−/−) mutant mice were tested in two aggression paradigms. In general, there was no significant difference in aggressiveness between WT and OT−/+ mice. However, there were significant reductions in the duration of aggressive behaviors among OT−/− animals, especially in agonistic encounters within neutral arenas. The OT−/− mice did not exhibit any sensorimotor deficits or display any altered general anxiety levels that may have accounted for the observed reduction in aggressive behavior. These data indicate that aggression is mediated in part by OT in mice and that increased aggressiveness is not an obligatory phenotypic result of targeted genetic disruption of any gene.

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Randy J. Nelson

The Ohio State University Wexner Medical Center

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Ning Zhang

The Ohio State University Wexner Medical Center

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Richard J. Traystman

University of Colorado Denver

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C. Sue Carter

Indiana University Bloomington

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