Ceftriaxone attenuates acquisition and facilitates extinction of cocaine-induced suppression of saccharin intake in C57BL/6J mice

Freet, Christopher S.; Lawrence, Antoneal L.

doi:10.1016/j.physbeh.2015.06.009

Cited by 6 publications

(4 citation statements)

References 45 publications

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“…Instead, we hypothesize that cocaine exposure induces long-lasting neuroplastic adaptations in the mesocorticolimbic system, responsible for natural reward processing, leading to the observed changes in saccharin preference. In line with this, previous studies have extensively documented that pairing cocaine with saccharin dramatically decreases saccharin intake 12 , 13 , 21 – 23 . This effect appears to be due to a decrease in the perceived value of saccharin as a reward, rather than an impairment in sweet taste sensitivity 13 .…”

Section: Discussionsupporting

confidence: 68%

Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition

Alegre-Zurano,

Caceres-Rodriguez,

Berbegal-Sáez

et al. 2023

Sci Rep

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A single dose of cocaine abolishes endocannabinoid-mediated long-term depression (eCB-LTD) in the nucleus accumbens (NAc) within 24 h of administration. However, it is uncertain whether this altered neuroplasticity entails a behavioral deficit. As previously reported, after a single dose of cocaine (20 mg/kg), mice displayed impaired eCB-LTD in the NAc. Such cocaine-induced neuroplastic impairment was accompanied by an altered preference for saccharin and social interactions and a reduction in mRNA levels of the anandamide-catabolizing enzyme NAPE-PLD. The pharmacological increase of anandamide through the fatty acid amide hydrolase (FAAH) inhibitor URB597 (1 mg/kg) reversed the cocaine-induced loss of eCB-LTD in the NAc and restored normal social interaction in cocaine-exposed mice, but it did not affect saccharin preference. Overall, this research underlines the neuroplastic and behavioral alterations occurring after the initial use of cocaine and suggests a potential role for anandamide.

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Section: Discussionsupporting

confidence: 68%

Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition

Alegre-Zurano,

Caceres-Rodriguez,

Berbegal-Sáez

et al. 2023

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Instead, we hypothesize that cocaine exposure induces long-lasting neuroplastic adaptations in the mesocorticolimbic system, responsible for natural reward processing, leading to the observed changes in saccharin preference. In line with this, previous studies have extensively documented that pairing cocaine with saccharin dramatically decreases saccharin intake 12,13,[21][22][23] . This effect appears to be due to a decrease in the perceived value of saccharin as a reward, rather than an impairment in sweet taste sensitivity 13 .…”

Section: Discussionsupporting

confidence: 64%

Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition

Zurano

Caceres-Rodriguez

Berbegal-Sáez

et al. 2023

Preprint

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Background: A single usage of a drug of abuse can have lasting effects on both the brain and behavior, continuing even after the drug has been metabolized and eliminated from the body. A single dose of cocaine can abolish endocannabinoid-mediated long-term depression (eCB-LTD) in the nucleus accumbens (NAc) within 24 hours of administration. However, it is uncertain whether this altered neuroplasticity entails a behavioral deficit. Methods: Our study employed adult male mice to investigate the effects of a single dose of cocaine (20 mg/kg) on eCB-LTD, saccharin preference, and social interactions 24 hours after administration. We also examined the gene expression in components of the eCB system. The pharmacological increase of anandamide was evaluated using the fatty acid amide hydrolase (FAAH) inhibitor URB597 (1 mg/kg). Results: After a single dose of cocaine, mice displayed altered plasticity, social interactions, and preference for saccharin and a reduction in mRNA levels of the anandamide-catabolizing enzyme NAPE-PLD. We discovered that the FAAH inhibitor URB597 (1 mg/kg) successfully reversed the cocaine-induced loss of eCB-LTD in the NAc and restored normal social interaction in cocaine-exposed mice, but it did not affect their saccharin preference. Conclusions: Overall, this research underlines the neuroplastic changes and subsequent behavioral alterations that occur after the initial use of cocaine, while also suggesting a potential role for anandamide in the early impairments caused by cocaine. The findings highlight the importance of understanding the mechanisms underlying the initiation of drug use and offer a potential therapeutic target.

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“…Thus, our results could indicate that mice exposed to repeated caffeine-mixed alcohol during adolescence may be at greater risk for future abuse of rewarding substances. To test this hypothesis, we investigated how repeated exposure to caffeine-mixed alcohol in adolescence would alter intake of a natural reward (saccharin) in adulthood [ 30 , 31 , 57 , 58 ]. In support of our hypothesis, we found that mice exposed to caffeine-mixed alcohol increased voluntary saccharin consumption and preference compared to water control mice ( Fig 7 ).…”

Section: Discussionmentioning

confidence: 99%

Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice

Robins

Rijn

2016

PLoS ONE

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The number of highly caffeinated products has increased dramatically in the past few years. Among these products, highly caffeinated energy drinks are the most heavily advertised and purchased, which has resulted in increased incidences of co-consumption of energy drinks with alcohol. Despite the growing number of adolescents and young adults reporting caffeine-mixed alcohol use, knowledge of the potential consequences associated with co-consumption has been limited to survey-based results and in-laboratory human behavioral testing. Here, we investigate the effect of repeated adolescent (post-natal days P35-61) exposure to caffeine-mixed alcohol in C57BL/6 mice on common drug-related behaviors such as locomotor sensitivity, drug reward and cross-sensitivity, and natural reward. To determine changes in neurological activity resulting from adolescent exposure, we monitored changes in expression of the transcription factor ΔFosB in the dopaminergic reward pathway as a sign of long-term increases in neuronal activity. Repeated adolescent exposure to caffeine-mixed alcohol exposure induced significant locomotor sensitization, desensitized cocaine conditioned place preference, decreased cocaine locomotor cross-sensitivity, and increased natural reward consumption. We also observed increased accumulation of ΔFosB in the nucleus accumbens following repeated adolescent caffeine-mixed alcohol exposure compared to alcohol or caffeine alone. Using our exposure model, we found that repeated exposure to caffeine-mixed alcohol during adolescence causes unique behavioral and neurochemical effects not observed in mice exposed to caffeine or alcohol alone. Based on similar findings for different substances of abuse, it is possible that repeated exposure to caffeine-mixed alcohol during adolescence could potentially alter or escalate future substance abuse as means to compensate for these behavioral and neurochemical alterations.

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Ceftriaxone attenuates acquisition and facilitates extinction of cocaine-induced suppression of saccharin intake in C57BL/6J mice

Cited by 6 publications

References 45 publications

Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition

Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition

Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition

Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice

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