Sensitization to social anxiolytic effects of ethanol in adolescent and adult Sprague–Dawley rats after repeated ethanol exposure

Adolescent alcohol use can lead to numerous consequences, including altered stress reactivity and higher risk for later anxiety and alcohol use disorders. Many studies have examined the consequences of heavy ethanol exposure in adolescence, but far less is understood about lower levels of intoxication. The present study examined moderate adolescent ethanol exposure as a possible factor in increasing stress reactivity in adulthood, measured through general and social anxiety-like behaviors, as well voluntary ethanol intake. Male and female Sprague–Dawley rats underwent an adolescent chronic intermittent ethanol (aCIE) vapor exposure during early adolescence, reaching moderate blood ethanol concentrations. Animals then underwent two days of forced swim stress in adulthood. We found that ethanol-exposed males consumed more ethanol than their air counterparts and an interesting stress and ethanol exposure interaction in males. There were no significant effects on voluntary drinking in females. However, the social interaction test revealed increased play-fighting behavior in ethanol-exposed females and reduced social preference in females after two days of stress exposure. Overall, this work provides evidence for sex-specific, long-term effects of moderate aCIE and susceptibility to acute stress in adulthood.

Download Full-text

7,8-Dihydroxyflavone Enhances Cue-Conditioned Alcohol Reinstatement in Rats

Brain Sciences ◽

10.3390/brainsci10050270 ◽

2020 ◽

Vol 10 (5) ◽

pp. 270 ◽

Cited By ~ 1

Author(s):

Samuel J. Hogarth ◽

Elvan Djouma ◽

Maarten van den Buuse

Keyword(s):

Body Weight ◽

Progressive Ratio ◽

Ethanol Exposure ◽

Ethanol Solution ◽

Female Rats ◽

Male Rats ◽

Sprague Dawley ◽

Self Administration ◽

Bdnf Expression ◽

Sprague Dawley Rats

Alcohol use disorder (AUD) is a detrimental disease that develops through chronic ethanol exposure. Reduced brain-derived neurotrophic factor (BDNF) expression has been associated with AUD and alcohol addiction, however the effects of activation of BDNF signalling in the brain on voluntary alcohol intake reinstatement and relapse are unknown. We therefore trained male and female Sprague Dawley rats in operant chambers to self-administer a 10% ethanol solution. Following baseline acquisition and progressive ratio (PR) analysis, rats were split into drug and vehicle groups during alcohol lever extinction. The animals received two weeks of daily IP injection of either the BDNF receptor, TrkB, agonist, 7,8-dihydroxyflavone (7,8-DHF), or vehicle. During acquisition of alcohol self-administration, males had significantly higher absolute numbers of alcohol-paired lever presses and a higher PR breakpoint. However, after adjusting for body weight, the amount of ethanol was not different between the sexes and the PR breakpoint was higher in females than males. Following extinction, alcohol-primed reinstatement in male rats was not altered by pretreatment with 7,8-DHF when adjusted for body weight. In contrast, in female rats, the weight-adjusted potential amount of ethanol, but not absolute numbers of active lever presses, was significantly enhanced by 7,8-DHF treatment during reinstatement. Analysis of spontaneous locomotor activity in automated photocell cages suggested that the effect of 7,8-DHF was not associated with hyperactivity. These results suggest that stimulation of the TrkB receptor may contribute to reward craving and relapse in AUD, particularly in females.

Download Full-text

Decreased Immunoreactivity of the Melanocortin Neuropeptide α-Melanocyte-Stimulating Hormone (α-MSH) After Chronic Ethanol Exposure in Sprague-Dawley Rats

Alcoholism Clinical and Experimental Research ◽

10.1111/j.1530-0277.2007.00578.x ◽

2008 ◽

Vol 32 (2) ◽

pp. 266-276 ◽

Cited By ~ 30

Author(s):

Montserrat Navarro ◽

Inmaculada Cubero ◽

Darin J. Knapp ◽

George R. Breese ◽

Todd E. Thiele

Keyword(s):

Ethanol Exposure ◽

Chronic Ethanol ◽

Sprague Dawley ◽

Melanocyte Stimulating Hormone ◽

Chronic Ethanol Exposure ◽

Sprague Dawley Rats ◽

Stimulating Hormone

Download Full-text

Effects of ethanol exposure during adolescence or in adulthood on Pavlovian conditioned approach in Sprague-Dawley rats

Alcohol ◽

10.1016/j.alcohol.2014.05.006 ◽

2014 ◽

Vol 48 (8) ◽

pp. 755-763 ◽

Cited By ~ 24

Author(s):

Alexander James McClory ◽

Linda Patia Spear

Keyword(s):

Ethanol Exposure ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Pavlovian Conditioned Approach ◽

Conditioned Approach

Download Full-text

Role of endotoxin in the hypermetabolic state after acute ethanol exposure

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.275.6.g1252 ◽

1998 ◽

Vol 275 (6) ◽

pp. G1252-G1258 ◽

Cited By ~ 21

Author(s):

Chantal A. Rivera ◽

Blair U. Bradford ◽

Vitor Seabra ◽

Ronald G. Thurman

Keyword(s):

Oxygen Uptake ◽

Kupffer Cells ◽

Ethanol Exposure ◽

Ethanol Administration ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Hypermetabolic State ◽

Acute Ethanol ◽

Eicosanoid Release

This study investigated the role of endotoxin in the hypermetabolic state or swift increase in alcohol metabolism (SIAM) due to acute ethanol exposure. Female Sprague-Dawley rats (100–120 g) were given ethanol (5 g/kg) by gavage. Endotoxin measured in plasma from portal blood was not detectable in saline-treated controls; however, 90 min after ethanol, endotoxin was increased to 85 ± 14 pg/ml, and endotoxin clearance was diminished by ∼50%. Oxygen uptake in perfused livers was increased 48% by ethanol, and production of PGE2 by isolated Kupffer cells was increased similarly. These effects were blunted by elimination of gram-negative bacteria and endotoxin with antibiotics before ethanol administration. To reproduce ethanol-induced endotoxemia, endotoxin was infused via the mesenteric vein at a rate of 2 ng ⋅ kg−1 ⋅ h−1. Endotoxin mimicked the effect of ethanol on oxygen uptake. The specific Kupffer cell toxicant GdCl3completely prevented increases in oxygen uptake due to endotoxin. These findings demonstrate that endotoxin plays a pivotal role in SIAM, most likely by stimulating eicosanoid release from Kupffer cells.

Download Full-text

The Role of Alcohol in Hippocampal Calcium Channel (Cav1.2) expression

Proceedings of IMPRS ◽

10.18060/24670 ◽

2020 ◽

Vol 3 ◽

Author(s):

Ryan Kokoska ◽

Eric Rodriguez ◽

Bryan Yamamoto

Keyword(s):

Calcium Signaling ◽

Regional Distribution ◽

Alcohol Exposure ◽

Chronic Alcoholism ◽

Ethanol Exposure ◽

Sprague Dawley ◽

Memory And Learning ◽

Disease States ◽

Stratum Pyramidale ◽

Sprague Dawley Rats

Background and Hypothesis: Voltage-gated L-type calcium channels (Cav1.2 and Cav1.3) in the hippocampus play important roles in glutamatergic neurotransmission underlying memory and learning. Their overexpression has been implicated in neuroexcitatory cell death and disease states including chronic alcoholism. While increases in Cav1.2 gene expression have been reported in the hippocampus after chronic ethanol exposure in rats, the regional distribution of Cav1.2 protein after voluntary ethanol (EtOH) drinking has not been reported. We hypothesize that the expression of Cav1.2 channels within the hippocampus is increased by EtOH drinking in a region-specific manner. Methods: Male Sprague Dawley rats were allowed 28 days of intermittent access to a 10% EtOH solution. At 24 hours after the last exposure to EtOH, brains were collected and processed for immunohistochemistry. Cav1.2 associated immunofluorescent signal from subregions of the hippocampus was quantified using ImageJ analysis software. Results: Immunohistochemical results indicate that Cav1.2 immunoreactivity in the hippocampal stratum granulosum layer within the Dentate Gyrus and the stratum pyramidale layer within CA1 and CA3 regions was increased in response to EtOH treatment. There was no significant change in Cav1.2 immunoreactivity for the CA2 region. Conclusion: This study suggests that calcium signaling in subregions of the hippocampus is differentially affected by EtOH consumption that may contribute to eventual calcium-mediated apoptosis. Impact and Implications: Understanding the process of EtOH-induced hippocampal calcium signaling presents opportunities for understanding the consequences of chronic alcohol exposure related to hippocampal function including memory and learning, and possible interventional therapies for alcohol damage.

Download Full-text