Week2 pharmacological and physiological antagonism

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Prior to beginning work on this discussion, read the required chapters from the text and review the required articles for this week. Alcohol and caffeine have nearly opposite effects on behavior and the nervous system, yet these substances are not used to treat overdose or addiction to the other. Why not use caffeine to treat alcohol addiction? Analyze the issues of pharmacological and physiological antagonism. Explain the receptor systems involved and the central nervous system structures effects with regard to this question. Frame your analysis in terms of drug action first and other consequences second.

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Response 1

· HI Class,

The question was asked about why we don’t treat alcohol addiction with caffeine. To answer that question, let’s investigate both and see if that would even be possible. We know that caffeine makes you stay awake and alert when you feel tired. Also, it can have other effects on you when you have too much. “Caffeine is the most consumed psychostimulant globally, and it is known to affect “fundamental human processes such as sleep, arousal, cognition and learning, and memory.” (Rivera-Oliver, M., & Díaz-Ríos, M. 2014). Another thing is that most drinks with alcohol add some caffeine to make certain drinks. So how could caffeine help treat alcohol addiction if we add them together? In one article I had read, the Rationale of the theory is that “Caffeine is commonly believed to offset the acute effects of alcohol, but some evidence suggests that cognitive process remains impaired when adding caffeine and alcohol together.” (Bailey, K et al., 2016) The statement that I just made before answers one question when you make them together, it does not matter, and you are still impaired. In the article By, Baily et al. did a study on this topic because people thought that mixing caffeine with alcohol would lessen the effects of the alcohol. The study used caffeine with placebo, alcohol with placebo, and alcohol and caffeine together. (Bailey, K et al. 2016) They found out that “alcohol did not abolish conflict monitoring and adaptation; however, caffeine eliminated conflict adaptation and mixed how the previous conflict affected the neural conflict monitoring response.”  (Bailey, K et al., 2016) They are saying that mixing the caffeine does not offset the alcohol. However, replacing caffeine with alcohol might mask the effects of alcohol. Still, I am not sure if replacing it is a good idea, so maybe we should look at the agonist’s and antagonists’ receptors and see if we can get the answer there.

· Analyze the issues of pharmacological and physiological antagonism

· Suppose we investigate caffeine receptors and what they might do first. Caffeine is a nonselective blocker of adenosine receptors A1, A2a, A2b, and A3, signaling the central nervous system. (Rivera-Oliver, M., & Díaz-Ríos, M. 2014). The use of caffeine can affect the activation or inhibition of A1 and A2a adenosine receptors as the main effect on the body for the person who has consumed the caffeine. “The seemingly paradoxical use of adenosine receptor agonists and antagonists to treat similar diseases suggests that factors such as dosage, extracellular concentrations of potential excitotoxic transmitters, and known anatomical and pharmacological relationship between adenosine and dopamine receptors as they influence glutamate release.” (Rivera-Oliver, M., & Díaz-Ríos, M. 2014). We know that caffeine affects the dopamine receptors, affecting that area. When looking at alcohol can affect what receptors. We know that alcohol can kill brain cells and the activity that they might have to perform. “GABAergic neurotransmission and GABAA receptors have long been implicated in mediating at least some of the pharmacological actions of alcohol.” (Paul, S.M 2006) Alcohol can affect other receptors, as in the dopamine D1 receptor agonist, the dopamine D1 receptor antagonist. (Ferré S, & O’Brien MC 2011) If you have noticed that both caffeine and alcohol affect dopamine. When a person is just on caffeine is a nonselective adenosine receptor antagonist. “A2a receptors can potentiate the effects of alcohol-induced dopamine release., and Chronic alcohol intake decreases adenosine tone.” (Ferré S, & O’Brien MC 2011) So we have seen what can be done to a person’s receptors by the effects of caffeine and alcohol.

·  So, look back and see if we can answer whether caffeine can be used for alcohol addiction. I read that a person is going through withdrawals that caffeine acts as a treatment by blocking the effects of the A1 receptors. (Ferré S, & O’Brien MC 2011) Other than that, I would not think we could treat with caffeine for alcohol addiction. A few reasons why that caffeine is can still cause damage to a person’s brain and body, just like alcohol, but in different ways. If a person drinks too much caffeine, they can become violent, just like some that have consumed too much alcohol. They both can be addictive and cause issues for the person involved. So I would say that we can not treat a person with alcohol addiction to caffeine.


Response 2

Terms of Drug Action

It is a branch of pharmacology that deals with the impact of medications on the body and the bacteria and other parasites that reside inside or on the body. It considers both drug action and drug impact, referring to both the immediate and long-term consequences of drug-receptor interaction. Pharmacological interventions aim to induce desirable effects with the appropriate time course while minimizing side effects. PK/PD modelling, based on the plasma concentration-response relationship, has been used to study the connection between the dosage delivered and the clinical response to various medications.

The molecular processes behind their interaction are not well known despite the widespread belief that caffeine counteracts the intoxicating effects of alcohol. Coffee and alcohol modify adenosine neurotransmission in a complicated and dose-dependent manner. Caffeine and alcohol are discussed in this article as a possible combination. No experiments in the lab are allowed because of ethical considerations, even if caffeine is used to simulate the extreme alcohol intoxication experienced by many young people in real-world circumstances (Heinz et al., 2020).

After ingesting caffeine orally, 99 per cent of it is absorbed from the digestive system within 45 minutes. Gender, genetics, liver illness, or drug or alcohol use have little effect on absorption. Caffeine is found in all body fluids, including blood, urine, saliva, and faeces. A single oral dosage of caffeine (4 mg/kg) results in peak plasma concentrations within 1–2 hours. Caffeine and its metabolites do not build up in the body’s organs or tissues.

Compulsive behavior may be reduced by using an antagonist, which prevents a drug’s postsynaptic effects from taking effect. The addict’s usage of the antagonist is causing the issue. A relapse into drug misuse will make the antagonist drug much more harmful if the addict does not continue to take it and relapses. According to our text, the tolerance built up with the substance of abuse will eventually wear off. Respiratory depression may occur if opiates are used again after an antagonist medication has been used (Garami et al., 2020).

It is called pharmacological antagonism when an antagonist interferes with the action of an antagonist by responding to the receptor or another component of the structure Antibodies with no additional pharmacological function is referred to as “competitive antagonists.” Alcohol’s significant pharmacological impact is the gradual, reversible depression that affects behavior, mental functioning, and cognition. Initially, the ingestion of modest dosages of alcohol stimulates respiration. Respiration slows down when the BAC level rises. Respiration ceases to be lethal at hazardous concentrations. An anti-convulsant known as alcohol isn’t used in this manner. Seizures are possible during the time of hyper-excitability that occurs with alcohol withdrawal.

Most people ingest caffeine as a stimulant for the central nervous system. Caffeine has been shown to have three primary modes of action on the central nervous system. Inhibition of certain phosphors and mobilization of intracellular calcium relieves discomfort. Only occur at very high doses of caffeine that have no physiological effect on the body. Methyl xanthine’s sole plausible mechanism of action is the inhibition of adenosine receptors. Caffeine causes relative hypoperfusion of the brain by increasing energy consumption while decreasing cerebral blood flow at the same time. Noradrenaline neurons seem to be activated by caffeine, and dopamine levels appear to be affected locally. The methyl xanthine’s impact on serotonin neurons may be responsible for many of the stimulatory effects of coffee. Methyl xanthine affects animals’ locomotors activity that is dose-dependent. Its psychedelic effects on humans, on the other hand, are generally modest and challenging to identify (Pillinger et al., 2019).

The methylxanthine impact on arousal, alertness, and exhaustion is responsible for the effects of caffeine on memory, learning, and performance. In addition, a person’s tolerance to the methylxanthine in caffeine directly impacts their anxiety and sleep patterns. However, children tend to be less vulnerable to the effects of methylxanthine than adults in general. Caffeine dependency and withdrawal symptoms have been documented. However, the central nervous system does not seem to acquire a high tolerance to its effects.

 

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