Alcohol Alters Rat Adrenomedullary Function and Stress Response

Abstract

Most alcohol researchers do not address the effects of intoxication on the sympatho-adrenomedullary system response to stressful situations. We previously determined that rats consuming nearly 9 g ethanol (EtOH) per kg body weight per day in liquid diet form for 1 week increased adrenal gene expression of enzymes for catecholamine synthesis that was further elevated by acute IMMO. We hypothesized that the response to chronic mild stressors would also be altered after consumption of lower concentrations of EtOH in drinking water. Two experiments were conducted: 10% w/v for 4 weeks or 6% w/v for 7 weeks +/- wire mesh restraint (WMR). These were compared with ad libitum (adlib) and pair-fed control rats. Adrenal gene expression of catecholamine synthesizing enzymes was assayed. Tyrosine hydroxylase gene expression was elevated 80% to 90% by alcohol consumption in both experiments (P < 0.001) compared with adlib control rats. Dopamine betab-hydroxylase and phenylethanolamine-N-methyl transferase gene expressions were unaffected by 10% alcohol (P > 0.05) but were increased by 6% alcohol (P < 0.01). WMR decreased already elevated gene expression of all three enzymes. Pair feeding to 6% EtOH drinkers also increased gene expression for the three enzymes but was decreased by WMR, although not to levels of adlib rats. Increased gene expression for adrenal synthesis of catecholamines in response to repeated alcohol consumption increases the likelihood that the subject can respond physiologically to acute or chronic stress. This may have life-saving consequences in humans and in animals known to consume fermented materials and may contribute to increased aggressive behavior.

Neurotoxic catecholamine metabolite in nociceptors contributes to painful peripheral neuropathy

“…As some forms of painful peripheral neuropathy (e.g. alcoholic peripheral neuropathy) are associated with marked increases in plasma catecholamines (Patterson‐Buckendahl et al. , 2004, 2005), we tested the hypothesis that metabolites of catecholamines contribute to ethanol‐induced painful peripheral neuropathy.…”

Independent contributions of alcohol and stress axis hormones to painful peripheral neuropathy

“…In summary, prior studies have established a role of neuroendocrine stress axis mediators from the sympathoadrenal and hypothalamic-pituitary-adrenal stress axes, to both the addictive (Adinoff et al, 1998, Gianoulakis, 1998, Adinoff et al, 2005, Devaud et al, 2006, Morrow et al, 2006, Richardson et al, 2008, Li et al, 2011, Evans et al, 2012, Prendergast and Mulholland, 2012, Vendruscolo et al, 2012) and neurotoxic (Silva et al, 2002, Patterson-Buckendahl et al, 2004, Patterson-Buckendahl et al, 2005, Dina et al, 2008a) effects of alcohol. However, prior experimental models have not allowed a distinction between the individual impact of alcohol and stress hormones.…”

Differentially co-expressed genes in postmortem prefrontal cortex of individuals with alcohol use disorders: influence on alcohol metabolism-related pathways

“…Studies using animal or cell culture models have shown that alcohol exposure alters the expression of genes involved in numerous cellular functions, including catecholamine metabolism (Patterson-Buckendahl et al 2004), signal transduction cascades (Fox et al 1996), or mitochondrial function and oxidative stress response (Chu et al 2007). Studies of postmortem brains from human AUD subjects demonstrated altered gene expression in specific brain regions, such as frontal and motor cortices (Lewohl et al 2000; Liu et al 2004; Liu et al 2006; MacKay et al 2011; Mayfield et al 2002).…”