Effects of ceftriaxone on ethanol drinking and GLT-1 expression in ethanol dependence and relapse drinking

Alcohol ◽  
2021 ◽  
Vol 92 ◽  
pp. 1-9
Author(s):  
William C. Griffin ◽  
Harold L. Haun ◽  
Vorani S. Ramachandra ◽  
Lori A. Knackstedt ◽  
Patrick J. Mulholland ◽  
...  
2019 ◽  
Author(s):  
William C. Griffin ◽  
Jennifer A. Rinker ◽  
John J. Woodward ◽  
Patrick J. Mulholland ◽  
Howard C. Becker

AbstractThe function of the ventral hippocampus (vHC) supports many behaviors, including those related to reward seeking behaviors and drug addiction. We used a mouse model of alcohol dependence and relapse to investigate the role of the vHC in alcohol (ethanol) drinking. One experiment used a chemogenetic approach to inhibit vHC function while ethanol dependent and non-dependent mice had access to ethanol. Interestingly, the non-dependent mice expressing an inhibitory DREADD in the VHC showed a significant increase in ethanol drinking (∼30%) after hM4Di DREADD activation with clozapine-n-oxide (CNO; 3 mg/kg, ip.) compared to vehicle. On the other hand, ethanol dependent mice, which were already drinking significantly more ethanol than non-dependent mice, only had a slight, non-significant increase in drinking after CNO challenge. In a separate group of dependent and non-dependent mice, GCaMP6f calcium-dependent activity was recorded in the vHC while mice were actively drinking ethanol. These data showed that once mice were rendered ethanol dependent and were drinking more ethanol than the non-dependent mice, calcium signaling in the ventral hippocampus decreased (∼45%) in the ethanol dependent mice compared to the non-dependent mice. Together, these findings suggest that ethanol dependence reduces activity of the ventral hippocampus and that reduced function of this brain region contributes to increased ethanol drinking.


2021 ◽  
Vol 187 ◽  
pp. 108497 ◽  
Author(s):  
Elizabeth A. Sneddon ◽  
Kristen M. Schuh ◽  
John W. Frankel ◽  
Anna K. Radke

1986 ◽  
Vol 378 (1) ◽  
pp. 107-114 ◽  
Author(s):  
Charles W. Wilkinson ◽  
John C. Crabbe ◽  
L. Donald Keith ◽  
John W. Kendall ◽  
Daniel M. Dorsa

2010 ◽  
Vol 35 (6) ◽  
pp. 1241-1252 ◽  
Author(s):  
Emily G Lowery ◽  
Marina Spanos ◽  
Montserrat Navarro ◽  
Angela M Lyons ◽  
Clyde W Hodge ◽  
...  
Keyword(s):  
Hpa Axis ◽  

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Fumihiko Sano ◽  
Tetsuya Ohira ◽  
Akihiko Kitamura ◽  
Hironori Imano ◽  
Renzhe Cui ◽  
...  

Background— Evidence on the relationship of a wide range of alcohol consumption with risk of incident atrial fibrillation has been limited. Methods— Between 1991 and 1995, 8602 Japanese men and women aged 30 to 80 years and free of clinical atrial fibrillation took part in the first examination of the Circulatory Risk in Communities Study(CIRCS)- a population based cohort study of cardiovascular risk factors, cardiovascular disease incidence, and their trends in Japanese communities. In the first examination, we checked a detailed medical history, physical examination, blood and urine examination, and electrocardiogram (ECG). An interviewer obtained histories in detail for weekly alcohol intake. In the follow-up period, incident atrial fibrillations were ascertained by annual ECG record and medical history of treatment of atrial fibrillation. ECGs were coded with the Minnesota Code by trained physician-epidemiologists. Differences in baseline characteristics between atrial fibrillation cases and controls were compared using Student t-tests or chi-squared tests. The hazard ratios (HRs) of incidence of atrial fibrillation and 95% confidence interval (CI) relative to the never-drinking group were calculated with adjustment for age and other potential confounding factors using the Cox proportional hazard model. Results— During an average follow-up of 6.4 years, 290 incident atrial fibrillation occurred. The higher incidence rate of atrial fibrillation was observed among participants with more than 69 g of ethanol drinking per week, compared with less than 69 g of ethanol drinking per week. On the other hand, light to moderate alcohol consumption was not associated with risk of atrial fibrillation. Compared with the never drinking group, the multivariable-adjusted HRs of past, light (<23 g), light moderate (23-46 g), moderate (46-69 g), and heavy (>69 g) drinking groups were 1.20 (95% CI, 0.61-2.35), 0.85 (95% CI, 0.57-1.27), 1.05 (95% CI, 0.63-1.75), 1.34 (95% CI, 0.78-2.32), and 2.92 (95% CI, 1.61-5.28), respectively. Conclusions— Heavy alcohol consumption was associated with the higher risk of atrial fibrillation, whereas there was no association of less than moderate alcohol consumption and atrial fibrillation.


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