You are encouraged to post your required replies earlier in the week to promote more meaningful interactive discourse in this discussion.
Evaluate your colleagueâ€s analysis. To what extent was he or she accurate? Please use your research to support your assertions. Did the analysis take into consideration all the required elements? What might your colleague consider which was not already included in the analysis?
1ST Porter
An antagonist directly blocks the postsynaptic effects of a drug and in doing so reduces the compulsive behavior that comes from the use of it (Advokat, 2014). The problem lies in the continued use of the antagonist by the addict. If the addict does not continue using the antagonist and relapses, then the drug of abuse will become even more dangerous than before being treated with the antagonist drug (Advokat, 2014). Our text states that the tolerance that was gained with the drug of abuse will have worn off. An example would be with opiates- using this drug again after using the antagonist drug can lead to respiratory depression (Advokat, 2014).
Opiate antagonist drugs that are used for treatment are naltrexone, naloxone and nalmefene (Advokat, 2014). The receptor involved in this process is the GABA-B receptor. Baclofen is the agonist which reduces the effects of certain drugs such as heroin alcohol and psychostimulants (Advokat, 2014). Some of the treatments that are being used in trials and tested in labs seem to have benefits such as Vigabatrin which is an anticonvulsant and blocks the enzyme that breaks down GABA, but also has drawbacks due to the side effects of the drug. This drug causes visual field defects according to our text and has not been approved here in the United States (Advokat, 2014).
Gabapentin is a drug that is used to inhibit the release of glutamate and relieves the symptoms of alcohol abuse such as convulsions. By stimulating the glutamate receptor subtype mGluR2/3, glutamate agonists reduce the release of glutamate and in turn this may prevent relapse (Advokat, 2014). Since these receptors are also found in the dopamine terminals there is a probability that the initial use of a drug could be reduced since dopamine is decreased at the same time (Advokat, 2014). The abuse of cannabis and alcohol produces behavioral reactions due to the fact that they both depress the central nervous system. Some of the effects include memory problems, sleep disruptions, motor impairments and neuropsychological dysfunctions (Advokat, 2014).
Advokat, C. D., Comaty, J. E., & Julien, R. M. (2014). Julien’s primer of drug action: A comprehensive guide to the actions, uses, and side effects of psychoactive drugs (13th ed.). New York, NY: Worth Publishers.
2nd Peluso
Pharmacological antagonism refers to the relationship between drugs in which an antagonist blocks the activity of an antagonist by reacting to the receptor or other part of the structure. The antagonist serves no other pharmacological purpose and may serve as a competitive or non-competitive antagonist. The graded reversible depression involved in the behavior, mental functioning and cognition is seen as the primary pharmacological effect of alcohol. At first respiration is stimulated by the consumption of low doses of alcohol. As BAC levels increase respiration becomes depressed. At toxic levels respiration ceases causing fatalities. Alcohol is also known as an anti- convulsant but it is not utilized in this way. Withdrawal from alcohol often involves periods of hyper-excitability in which seizures may occur. (Advokat, C. D. Pg 132-134)
Ethanol is a very potent inhibitor of the function of the NMDA sub-type of glutamate receptors and glutamate receptor mediated synaptic plasticity . Ethanol is also known to disrupt glutaminergic neuro-transmission by the depression of the responsiveness of the NMDA receptor to the released glutamate. Ethanol inhibition of glutamate receptors seem to reconstruct itself in certain areas within the structure of the brain. These structures include the hippocampus, amygdala, and straitium. This requires high concentrations of the drug . This action provides the explanation as to the consequences surrounding severe intoxication are so severe. (Advokat, C. D. 132-134)
There is also research regarding the role that serotonin plays in the actions and effects of severe alcohol consumption and how alcohol reacts as a mediator to the reward , preference and cravings involved in the chronic use of alcohol. Studies have continued to show that chronic alcohol intake often results in augmentation of serotoninergic activity and serotonin dysfunction has been shown to play a role in the patho-genesis of certain types of alcoholism. The present emphasis regarding this issue involves the role that 5-HT2 and 5HT3 receptors regarding alcohols CNS effects on the body. (Advokat, C. D. Pg. 132 -136).
Physiological antagonism is the description of the behavior of a substance that produces effects which counteract those of another substance by using the mechanism that does not involve binding itself to the same receptor. Common clinical effects of alcohol intake includes increased sociability and excessive talking. There is also a decrease in inhibition and diminished attention span. Judgement and self control are also severely impaired and memory and concentration may be decreased as well. Chronic alcohol intake is also associated with cognitive deficits that often remain even after long periods of abstinence. This offers legitimate support to the fact that cognitive deficits in detoxified individuals are often due to damage within the frontal lobes of the brain. (Advokat, C. D. Pg. 132-136)
Advokat, C. D. (2014). Julien’s Primer of Drug Action. Thirteenth Edition. Worth Publishing.
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