A history of ethanol intake accelerates the development of morphine analgesic tolerance: A protective potential for omega-3 fatty acids.

Abstract

Adolescence is a critical life period during which significant neurodevelopmental changes occur within the central nervous system. Consistently, substance abuse in this stage has been found to induce persistent changes in brain responsiveness to future drug challenges. Nowadays, heavy episodic alcohol consumption during adolescence, also known as binge-drinking behavior, is a growing concern in modern societies. On the other hand, alcohol is well known to act as a gateway drug, that is, it promotes the individual's craving for consumption of other drugs of abuse. With this in mind, we aimed to assess whether adolescent ethanol exposure could alter the development of tolerance and dependence to morphine, as an available common opioid drug. Tail flick test was used to measure thermal nociceptive changes in adult male Wistar rats undergone ethanol/vehicle exposure during adolescence. Furthermore, morphine withdrawal syndrome was induced by naloxone injection, and behavioral signs were recorded for 20 min. It was found that adolescent ethanol intake facilitates morphine analgesic tolerance and decreases baseline latency; however, the severity of dependence is not significantly altered. Moreover, we found that 15 days of treatment with omega-3 fatty acids (O3) prevents the mentioned ethanol-induced changes suggesting a therapeutic potential for this compound. O3 supplementation, as an inexpensive and noninvasive method, may assist the clinicians to reverse the adverse effect of alcohol binge drinking on adolescents' brains and to reduce the vulnerability to drug exposure in adulthood.

Oral administration of coenzyme Q10 ameliorates memory impairment induced by nicotine-ethanol abstinence through restoration of biochemical changes in male rat hippocampal tissues

“…In is now well-established that both nicotine and alcohol abstinence following prolonged intake impairs various dysfunctions with a marked adverse effect on learning and memory 33 , 44 , 45 , 59 , 60 . Studies on human populations have revealed that nicotine-alcohol interaction further complicates the post-quit behavioral outcomes, therefore, finding therapeutic or ameliorative strategies are of paramount significance 61 – 63 .…”

Omega‐3 fatty acids supplementation prevents learning and memory impairment induced by chronic ethanol consumption in adolescent male rats through restoration of inflammatory and oxidative responses

“…In addition, O 3 treatment was done from PNDs 21 to 63 in parallel with behavioral tests. It should be mentioned that O 3 doses were chosen based on our previous studies (Ahmadi-Soleimani, Amiry, et al, 2023;Ahmadi-Soleimani, Azizi, et al, 2023;Amiry et al, 2023). The rats were randomly divided into six groups (n = 10 per group) and treated as follows:…”