Neurobiological mechanisms contributing to alcohol–stress–anxiety interactions

Abstract

This article summarizes the proceedings of a symposium that was presented at a conference entitled "Alcoholism and Stress: A Framework for Future Treatment Strategies". The conference was held in Volterra, Italy on May 6-9, 2008 and this symposium was chaired by Jeff L. Weiner. The overall goal of this session was to review recent findings that may shed new light on the neurobiological mechanisms that underlie the complex relationships between stress, anxiety, and alcoholism. Dr. Danny Winder described a novel interaction between D1 receptor activation and the CRF system Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptAlcohol. Author manuscript; available in PMC 2010 November 1. Published in final edited form as:Alcohol.

Evidence Revealing Deregulation of The KLF11-Mao A Pathway in Association with Chronic Stress and Depressive Disorders

“…In addition, it is likely that compounds to modulate the levels of expression and function of the KLF11-MAO-mediated pathway may increase neuroprotection, neuroplasticity, and synaptic activities. Maximizing the therapeutic effects upon these targets is also essential toward achieving comprehensive management of stress-induced, frequently treatmentresistant, psychiatric illnesses, and addictions (Barr et al, 2004;Beasley et al, 2005;Dwivedi et al, 2006;Frazer, 1997;Mitchell et al, 2012;Sanacora, 2008;Sawada et al, 2005;Silberman et al, 2009;Wallace et al, 2007). Thus, the new knowledge generated by the current study has mechanistic relevance and also provides the rationale for targeting this pathway to develop potential novel therapeutics approaches in the treatment of MDD.…”

Effects of a stressor and corticotrophin releasing factor on ethanol deprivation-induced ethanol intake and anxiety-like behavior in alcohol-preferring P rats

“…Brain regions implicated in CRF-induced and ethanol withdrawal-induced anxiety-like behavior are the amygdala (Amyg) (Huang et al 2010;Knapp et al 2007;Koob 2003Koob , 2008Lack et al 2008;Overstreet et al 2006;Rassnick et al 1993;Wand 2005;Silberman et al 2009) and the dorsal raphe nucleus (DRN) (Huang et al 2010;Overstreet et al 2006). The basolateral amygdala and dorsal bed nucleus of the stria terminalis were also implicated in withdrawalinduced anxiety-like behavior following repeated CRF and stressor presentations prior to exposure to chronic ethanolcontaining diets (Huang et al 2010).…”

“…Historically, the role of stress and stressors in elevated ethanol drinking in humans and animals has been controversial (e.g., Champagne and Kirouac 1987;Chester et al 2004;Lynch et al 1999;Pohorecky 1990Pohorecky , 1991Silberman et al 2009). Our laboratory demonstrated a reliable stressor-induced elevation of ethanol intake during deprivation periods (an elevated "alcohol deprivation effect" or ADE, Sinclair and Senter 1968) that preceded renewed ethanol availability in alcohol-preferring P rats Overstreet et al 2007).…”

The Neurobiology of Substance Use Disorders: Information for Assessment and Clinical Treatment

“…Clearly, this complex interaction of factors is compounded in co-occurring conditions, such as SUD and major depression (Niciu et al, 2009), SUD and anxiety disorders (Silberman et al, 2009), and SUD and trauma (Brady, Back, & Coffey, 2004). According to Brady et al (2004), epidemiological studies reveal a particularly high prevalence of SUD among individuals with PTSD; 36% to 50% of individuals seeking treatment for SUD have a lifetime prevalence of PTSD, and 25% to 42% have post-traumatic stress disorder (PTSD) at the time of treatment.…”