Vasopressin and alcohol: a multifaceted relationship

Harper, Kathryn M.; Knapp, Darin J.; Criswell, Hugh E.; Breese, George R.

doi:10.1007/s00213-018-5099-x

Cited by 27 publications

(17 citation statements)

References 167 publications

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“…The comprehensive and accurate characterization of transcriptional activity represents an important step in the understanding of chronic alcohol exposure in which gene expression occurs in the hypothalamic neurons. Many studies, including ours, have found that chronic alcohol drinking resulted in persistent changes in cytoplasmic mRNA levels of opioid and stress genes in rodent hypothalamus . In the present study, we hypothesized that alcohol‐induced transcriptional regulation in the nucleus is the critical step for maintaining the persistent changes in cytoplasmic mRNA levels and then subsequent peptide activity that is critically involved in excessive alcohol drinking.…”

Section: Discussionmentioning

confidence: 78%

“…Many studies, including ours, have found that chronic alcohol drinking resulted in persistent changes in cytoplasmic mRNA levels of opioid and stress genes in rodent hypothalamus. 11,15,19 In the present study, we hypothesized that alcohol-induced transcriptional regulation in the nucleus is the critical step for maintaining the persistent changes in cytoplasmic mRNA levels and then subsequent peptide activity that is critically involved in excessive alcohol drinking. Therefore, we investigated the effects of chronic alcohol and acute withdrawal on opioid and stress gene expressions at nuclear transcriptional activity in the hypothalamus.…”

Section: Discussionmentioning

confidence: 95%

“…Of interest, in a recent human genetic study, rs7913179 variant in the Avpi1 gene is found to associate with alcohol dependency in a genome‐wide gene‐by‐alcohol dependence interaction analysis in European men . Although the AVP/V1b receptor system plays important roles in alcohol drinking, it seems unknown, however, whether and how the hypothalamic AVP‐induced protein 1 is involved in alcohol drinking behaviors, and further study is needed.…”

Section: Discussionmentioning

confidence: 99%

“…Results from both clinic and preclinical studies have showed profound alterations of stress responsive systems after chronic alcohol abuse. Specifically, alcohol has direct or downstream effects on several hypothalamic stress‐responsive systems, including arginine vasopressin (AVP), oxytocin, corticotrophin releasing hormone (CRH) and their receptors, dynorphin and the kappa opioid receptors (KOP‐r) . The studies in both humans and rodents also provide clear support for the importance of these stress responsive systems in the process of alcohol consumption with strong interactions with hypothalamic‐pituitary‐adrenal (HPA) hormones and their receptors (eg, glucocorticoid receptors), especially after stress .…”

Section: Introductionmentioning

confidence: 99%

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Nuclear transcriptional changes in hypothalamus of Pomc enhancer knockout mice after excessive alcohol drinking

Zhou

Liang

Low

et al. 2019

Genes Brain and Behavior

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Persistent alterations of proopiomelanocortin (Pomc) and mu‐opioid receptor (Oprm1) activity and stress responses after alcohol are critically involved in vulnerability to alcohol dependency. Gene transcriptional regulation altered by alcohol may play important roles. Mice with genome‐wide deletion of neuronal Pomc enhancer1 (nPE1−/−), had hypothalamic‐specific partial reductions of beta‐endorphin and displayed lower alcohol consumption, compared to wildtype littermates (nPE1+/+). We used RNA‐Seq to measure steady‐state nuclear mRNA transcripts of opioid and stress genes in hypothalamus of nPE1+/+ and nPE1−/− mice after 1‐day acute withdrawal from chronic excessive alcohol drinking or after water. nPE1−/− had lower basal Pomc and Pdyn (prodynorphin) levels compared to nPE1+/+, coupled with increased basal Oprm1 and Oprk1 (kappa‐opioid receptor) levels, and low alcohol drinking increased Pomc and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1. In nPE1+/+, excessive alcohol intake increased Pomc and Oprm1, with no effect on Pdyn or Oprk1. For stress genes, nPE1−/− had lowered basal Oxt (oxytocin) and Avp (arginine vasopressin) that were restored by low alcohol intake to basal levels of nPE1+/+. In nPE1+/+, excessive alcohol intake decreased Oxt and Avpi1 (AVP‐induced protein1). Functionally examining the effect of pharmacological blockade of mu‐opioid receptor, we found that naltrexone reduced excessive alcohol intake in nPE1+/+, but not nPE1−/−. Our results provide evidence relevant to the transcriptional profiling of the critical genes in mouse hypothalamus: enhanced opioid and reduced stress gene transcripts after acute withdrawal from excessive alcohol may contribute to altered reward and stress responses.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nuclear transcriptional changes in hypothalamus of Pomc enhancer knockout mice after excessive alcohol drinking

Zhou

Liang

Low

et al. 2019

Genes Brain and Behavior

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“…Alcohol abuse is believed to contribute to the onset of over 60 types of diseases and injuries and a cause of at least 200 others at the same time [6]. Excessive alcohol consumption leads to the severe failures of digestive, cardiovascular, and nervous (central and peripheral) systems [6][7][8][9][10]. The most frequent disorders related to alcohol abuse include alcoholic liver disease (including steatosis, steatohepatitis, cirrhosis, or hepatocellular carcinoma), pancreatitis, gastritis, hypertension, arrhythmia, or cardiomyopathy [11][12][13][14][15][16][17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options

et al. 2020

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Purpose of the Review Alcohol abuse causes a wide range of disorders that affect the nervous system. These include confusion, cerebellar ataxia, peripheral neuropathy, and cognitive impairment. Chronic and excessive alcohol consumption is the primary cause of peripheral neuropathy. It is worth noting that peripheral neuropathy has no reliable treatment due to the poor understanding of its pathology. Recent Findings Coasting is a major feature of alcoholic neuropathy, largely due to chronic alcohol abuse. Its major features are hyperalgesia, allodynia, and burning pain. Even though much research was done in this area, still we do not have a full understanding of the mechanism of alcoholic neuropathy. However, some theories have been proposed. These include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy. The goal of treatment is to impede further damage to the peripheral nerves while also restoring their normal physiology. Alcohol abstinence, intake of balanced diets, and treatment with medications are suggested including benfotiamine, alpha-lipoic acid, acetyl-l-carnitine, vitamin E, methylcobalamin, myo-inositol, N-acetylcysteine, capsaicin, tricyclic antidepressants, or antiepileptic drugs. Summary This review focuses on the many pathways that play a role in the onset and development of alcohol-induced neuropathy, as well as present the possible treatment strategies of this disorder, providing insights into a further search of new treatment modalities.

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