Nicole M Enman

Temple University, Philadelphia, Pennsylvania, United States

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Publications (3)6.04 Total impact

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    ABSTRACT: Repeated, extreme, or traumatic stressors can elicit pathological effects leading to many negative physical and psychological outcomes. Stressors can precipitate the onset of psychiatric diseases, or exacerbate pre-existing disorders including various anxiety and mood disorders. As stressors can negatively impact human psychiatric health, it is essential to identify neurochemicals that may confer protection from the negative sequelae of repeated or extreme stress exposure. Elucidating the neurobiological underpinnings of stress resilience will enhance our ability to promote resilience to, or recovery from, stress-related psychiatric disease. Herein, we will review the evidence for neuropeptide Y as an endogenous mediator of resilience and its potential relevance for the treatment of stress-related psychiatric diseases.
    Neurobiology of stress. 01/2015; 1:33-43.
  • Nicole M Enman, Yong Zhang, Ellen M Unterwald
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    ABSTRACT: Posttraumatic stress disorder (PTSD) co-occurs highly with substance use disorders (SUD), yet the neurobiological basis for this comorbid relationship remains unclear. PTSD and SUDs result in similar pathological states including impulsive behavior, reward deficiency, and heightened stress sensitivity. Hence, PTSD and SUD may depend on overlapping dysfunctional neurocircuitry. Here we provide a short overview of the relationship between comorbid PTSD and SUD, as well as the potential role of select neurotransmitter systems that may underlie enhanced vulnerability to drug abuse in the context of PTSD.
    Pharmacology Biochemistry and Behavior 12/2013; · 2.82 Impact Factor
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    Nicole M Enman, Ellen M Unterwald
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    ABSTRACT: Glycogen synthase kinase 3 (GSK3) is implicated in mediating dopamine-dependent behaviors. Previous studies have demonstrated the ability of amphetamine, which increases extracellular dopamine levels and influences behavior, to regulate the activity of GSK3. This study used valproic acid and the selective GSK3 inhibitor, SB 216763, to examine the role of GSK3 in amphetamine-induced hyperactivity and the development of sensitized stereotypic behavior. Pretreatment with valproic acid (50-300 mg/kg, i.p.) or SB 216763 (2.5-5 mg/kg, i.p.) prior to amphetamine (2 mg/kg, i.p.) significantly reduced amphetamineinduced ambulation and stereotypy. To assess the development of sensitization to the stereotypic effects of amphetamine, mice were pretreated daily with valproic acid (300 mg/kg) or SB 216763 (5 mg/kg) prior to amphetamine (2 mg/kg) for 5 days. Upon amphetamine challenge (1 mg/kg) 7 days later, mice pretreated with valproate or SB 216763 showed a significant attenuation of amphetamine-induced sensitization of stereotypy. To determine whether regulation of GSK3 activity was associated with attenuation of acute amphetamine-induced hyperactivity by valproic acid, valproate (300 mg/kg) or vehicle was injected prior to amphetamine (2 mg/kg) or saline and brain tissue obtained. Analysis of the levels of phospho-GSK3α and β by immunoblot indicated that valproate increased phosphorylation of ser²¹-GSK3α in the frontal cortex, as well as ser⁹-GSK3β in the frontal cortex and caudate putamen of amphetamine-injected mice. These data support a role for GSK3 in acute amphetamine-induced hyperactivity and the development of sensitization to amphetamine-induced stereotypy.
    Behavioural brain research 05/2012; 231(1):217-25. · 3.22 Impact Factor