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In the 1960s, drugs categorized as benzodiazepines (BZO) started to be widely prescribed. These drugs are prescribed to treat anxiety and insomnia, alcohol withdrawal, and other conditions. These drugs could be addictive and they cause addiction in a way similar to that of opioids, cannabinoids, and the club drug gamma-hydroxybutyrate (GHB). Through specific actions on target GABA receptors, BZO result in a lessening of GABA restraint on the dopaminergic neurons and an increase in dopamine release.1
Research indicates that benzodiazepines weaken the influence of a group of cells, called inhibitory interneurons, in the brain’s ventral tegmental area (VTA). These neurons normally help prevent excessive dopamine levels by downregulating the firing rates of dopamine-producing neurons. Two negatives make a positive, so when benzodiazepines limit the interneurons’ restraining influence, the dopamine-producing neurons release more dopamine. Benzodiazepines’ newly discovered mechanism for producing reward is comparable to those of opiates, cannabinoids, and GHB. Each of the four drugs reduces an inhibitory influence on dopamine-producing cells, thereby promoting dopamine surges.
Barbiturates are synthetic drugs used in medicine to depress the central nervous system. Barbiturates were synthesized in 1864 by Adolf von Baeyer. The process was then perfected by the French chemist Edouard Grimaux in 1879. The effects range from mild sedation to coma and they may be used for sedation, sleep induction and hypnosis. Some barbiturates are used to relieve tension or anxiety prior to surgery and some are used as an adjunct to anesthesia. Historically, barbiturates were used as sedatives or hypnotics to relieve insomnia, but to date they are generally only used to treat extreme and serious cases of insomnia and to control seizures in epilepsy. Barbiturates that are used in controlling seizures and acute convulsions include phenobarbitone. The primary mechanism of action of barbiturates is inhibition of the central nervous system by stimulating the inhibitory neurotransmitter system in the brain called the [gamma]-aminobutyric acid (GABA) system. The GABA channel is a chloride channel that has five cells at its gate. When barbiturates bind to the GABA channel they lead to prolonged opening of the channel letting in Chloride ions into the cells in the brain. This leads to increased negative charge and alters the voltage in the brain cells. This change in voltage makes the brain cells resistant to nerve impulses and thus depresses them.1,2
The Use and Abuse of Benzodiazepines
More than 30 percent of overdoses involving opioids also involve benzodiazepines, sedatives commonly prescribed for anxiety or to help with insomnia. As stated, earlier, benzodiazepines work to calm or sedate a person, by raising the level of the inhibitory neurotransmitter GABA in the brain. Common benzodiazepines include diazepam (Valium), alprazolam (Xanax), and clonazepam (Klonopin),among others. Benzodiazepines, such as sedatives and sleeping aids, are often used for the short-term treatment of anxiety and insomnia. Benzodiazepine use is highly prevalent among U.S. adults. Benzodiazepine use disorders are relatively rare among the adults who use benzodiazepine medications, even if they are misusing them.
Barbiturates depress the central nervous system and have effects that are similar to those of alcohol. The immediate effects associated with taking barbiturates include, feelings of well-being or euphoria, reduced inhibitions, relaxation and sedation, lethargy and unconsciousness in higher doses.
Long-term use and abuse of barbiturates can lead to a number of different complications, including breathing difficulties, sexual dysfunction, shortened attention span, Short- and long-term memory loss and the development of physical dependence. Physical dependence develops over time with consistent barbiturate use. Physical dependence often arises in parallel with both tolerance (the need to use a higher dose of the drug to achieve the same effects that were once achieved at lower doses) and withdrawal (a series of negative psychological and physical symptoms that occur when levels of the drug in the system rapidly decrease).2,3
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