scholarly journals Encoding of the Intent to Drink Alcohol by the Prefrontal Cortex is blunted in Rats with a Family History of Excessive Drinking

2018 ◽  
Author(s):  
David N. Linsenbardt ◽  
Nicholas M. Timme ◽  
Christopher C. Lapish

The prefrontal cortex plays a central role in guiding decision-making, and its function is altered by alcohol use and an individual’s innate risk for excessive alcohol drinking. The primary goal of this work was to determine how neural activity in the prefrontal cortex guides the decision to drink. Towards this goal, the within-session changes in neural activity were measured from medial prefrontal cortex (mPFC) of rats performing a drinking procedure that allowed them to consume or abstain from alcohol in a self-paced manner. Recordings were obtained from rats that either lacked or expressed an innate risk for excessive alcohol intake - Wistar or Alcohol Preferring ‘P’ rats, respectively. Wistar rats exhibited patterns of neural activity consistent with the intention to drink or abstain from drinking, whereas these patterns were blunted or absent in P rats. Collectively, these data indicate that neural activity patterns in mPFC associated with the intention to drink alcohol are influenced by innate risk for excessive alcohol drinking. This observation may indicate a lack of control over the decision to drink by this otherwise well-validated supervisory brain region.

2020 ◽  
Vol 375 (1799) ◽  
pp. 20190231 ◽  
Author(s):  
David Tingley ◽  
Adrien Peyrache

A major task in the history of neurophysiology has been to relate patterns of neural activity to ongoing external stimuli. More recently, this approach has branched out to relating current neural activity patterns to external stimuli or experiences that occurred in the past or future. Here, we aim to review the large body of methodological approaches used towards this goal, and to assess the assumptions each makes with reference to the statistics of neural data that are commonly observed. These methods primarily fall into two categories, those that quantify zero-lag relationships without examining temporal evolution, termed reactivation , and those that quantify the temporal structure of changing activity patterns, termed replay . However, no two studies use the exact same approach, which prevents an unbiased comparison between findings. These observations should instead be validated by multiple and, if possible, previously established tests. This will help the community to speak a common language and will eventually provide tools to study, more generally, the organization of neuronal patterns in the brain. This article is part of the Theo Murphy meeting issue ‘Memory reactivation: replaying events past, present and future’.


2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Yu-Ruey Liu ◽  
Disline Manli Tantoh ◽  
Chuan-Chao Lin ◽  
Chih-Hsuan Hsiao ◽  
Yung-Po Liaw

Abstract Background Gout stems from both modifiable and genetic sources. We evaluated the risk of gout among Taiwanese adults with aldehyde dehydrogenase-2 (ALDH2) rs671 single nucleotide polymorphism (SNP) according to body mass index (BMI) and alcohol drinking. Methods We obtained information of 9253 individuals having no personal history of cancer from the Taiwan Biobank (2008–2016) and estimated the association between gout and independent variables (e.g., rs671, BMI, and alcohol drinking) using multiple logistic regression. Results Alcohol drinking and abnormal BMI were associated with a higher risk of gout whereas the rs671 GA+AA genotype was associated with a lower risk. The odds ratios (ORs) and 95% confidence intervals (CIs) were 1.297 and 1.098–1.532 for alcohol drinking, 1.550 and 1.368–1.755 for abnormal BMI, and 0.887 and 0.800–0.984 for GA+AA. The interaction between BMI and alcohol on gout was significant for GG (p-value = 0.0102) and GA+AA (p-value = 0.0175). When we stratified genotypes by BMI, alcohol drinking was significantly associated with gout only among individuals with a normal BMI (OR; 95% CI = 1.533; 1.036–2.269 for GG and 2.109; 1.202–3.699 for GA+AA). Concerning the combination of BMI and alcohol drinking among participants stratified by genotypes (reference, GG genotype, normal BMI, and no alcohol drinking), the risk of gout was significantly higher in the following categories: GG, normal BMI, and alcohol drinking (OR, 95% CI = 1.929, 1.385–2.688); GG, abnormal BMI, and no alcohol drinking (OR, 95% CI, = 1.721, 1.442–2.052); GG, abnormal BMI, and alcohol drinking (OR, 95% CI = 1.941, 1.501–2.511); GA+AA, normal BMI, and alcohol drinking (OR, 95% CI = 1.971, 1.167–3.327); GA+AA, abnormal BMI, and no alcohol drinking (OR, 95% CI = 1.498, 1.256–1.586); and GA+AA, abnormal BMI, and alcohol drinking (OR, 95% CI = 1.545, 1.088–2.194). Conclusions Alcohol and abnormal BMI were associated with a higher risk of gout, whereas the rs671 GA+AA genotype was associated with a lower risk. Noteworthy, BMI and alcohol had a significant interaction on gout risk. Stratified analyses revealed that alcohol drinking especially among normal-weight individuals might elevate the risk of gout irrespective of the genotype.


Science ◽  
2019 ◽  
Vol 366 (6468) ◽  
pp. 1008-1012 ◽  
Author(s):  
Cody A. Siciliano ◽  
Habiba Noamany ◽  
Chia-Jung Chang ◽  
Alex R. Brown ◽  
Xinhong Chen ◽  
...  

What individual differences in neural activity predict the future escalation of alcohol drinking from casual to compulsive? The neurobiological mechanisms that gate the transition from moderate to compulsive drinking remain poorly understood. We longitudinally tracked the development of compulsive drinking across a binge-drinking experience in male mice. Binge drinking unmasked individual differences, revealing latent traits in alcohol consumption and compulsive drinking despite equal prior exposure to alcohol. Distinct neural activity signatures of cortical neurons projecting to the brainstem before binge drinking predicted the ultimate emergence of compulsivity. Mimicry of activity patterns that predicted drinking phenotypes was sufficient to bidirectionally modulate drinking. Our results provide a mechanistic explanation for individual variance in vulnerability to compulsive alcohol drinking.


2002 ◽  
Vol 19 (1) ◽  
pp. 13-15 ◽  
Author(s):  
Alistair James ◽  
Guy Edwards

AbstractObjectives: To identify excessive drinking in a Hampshire general practice and evaluate the usefulness of the screening tools employed. Although excessive alcohol consumption is common, only one in 10 heavy drinkers is known to their general practitioner. Early identification of such patients increases the likelihood that successful intervention will decrease their alcohol intake. Screening helps recognise excessive drinkers.Method: Three hundred and one patients consulting their general practitioner for any reason were interviewed using a questionnaire comprising a drinking history, CAGE, and brief MAST (Michigan Alcohol Screening Test). The medical records of patients identified as drinking excessively were reviewed.Results: Forty-eight (15.9%) patients were identified as drinking to excess. Only nine of them were known to the general practitioner. The most useful tests were the drinking history and CAGE, detecting 21 and 20 of the excessive drinkers respectively. No single test used in isolation performed adequately, but the combination of a drinking history, including enquiry about binge drinking, and the CAGE was the most productive.Conclusion: Screening for excessive drinking by taking a simple drinking history and using the CAGE is cheap and easy to administer. Only about one in five of the patients identified in this study had information concerning excessive alcohol intake in their GP records.


2019 ◽  
Author(s):  
Daniel W. Bloodgood ◽  
Dipanwita Pati ◽  
Melanie M. Pina ◽  
Sofia Neira ◽  
J. Andrew Hardaway ◽  
...  

AbstractExcessive alcohol drinking has been shown to modify brain circuitry to predispose individuals for future alcohol abuse. Previous studies have implicated the central nucleus of the amygdala (CeA) as an important site for mediating the somatic symptoms of withdrawal and for regulating alcohol intake. In addition, recent work has established a role for both the Kappa Opioid Receptor (KOR) and its endogenous ligand dynorphin in mediating these processes. However, it is unclear whether these effects are due to dynorphin or KOR arising from within the CeA itself or other input brain regions. To directly examine the role of preprodynorphin (PDYN) and KOR expression in CeA neurons, we performed region-specific conditional knockout of these genes and assessed the effects on the Drinking in the Dark (DID) and Intermittent Access (IA) paradigms. We then examined the effects of DID on PDYN and KOR modulation of CeA circuit physiology. Conditional gene knockout resulted in sex-specific responses wherein PDYN knockout decreased alcohol drinking in both male and female mice, whereas KOR knockout decreased drinking in males only. We also found that neither PDYN nor KOR knockout protected against anxiety caused by alcohol drinking. Lastly, a history of alcohol drinking did not alter synaptic transmission in PDYN neurons in the CeA of either sex, but excitability of PDYN neurons was increased in male mice only. Taken together, our findings indicate that PDYN and KOR signaling in the CeA plays an important role in regulating excessive alcohol consumption and highlight the need for future studies to examine how this is mediated through downstream effector regions.


eNeuro ◽  
2019 ◽  
Vol 6 (4) ◽  
pp. ENEURO.0489-18.2019 ◽  
Author(s):  
David N. Linsenbardt ◽  
Nicholas M. Timme ◽  
Christopher C. Lapish

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