Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents.

By Day 6 Respond to two colleagues in one of the following ways: If your colleagues’ posts influenced your understanding of these concepts, be sure to share how and why. Include additional insights you gained. If you think your colleagues might have misunderstood these concepts, offer your alternative perspective and be sure to provide an explanation for them. Include resources to support your perspective. chiomas post Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents. The agonist-to-antagonist spectrum of action of psychopharmacologic agents occurs when a drug that is being used, enforces on the central receptor; and creates the movement of the ions through the leading receptor site (Stahl, 2013). An agonist refers to a chemical that binds to a receptor site when the receptor is activated, and it produces a biological response. Agonists can be full or partial. A full agonist has the efficacy to create a complete response while a partial agonist has lower efficacy and cannot produce a full response. Some examples of a full agonist are oxycodone, hydrocodone, and morphine, as they activate the brain’s opioid receptors, causing a full opioid effect (NIDA, 2018). Agonist drugs affect neuronal communication by boosting a natural full agonist neurotransmitter (Stahl, 2013). A partial agonist causes a lesser response while occupying all receptors. An example of a partial agonist is buprenorphine, as it can block the action of the neural neurotransmitters’ agonist but not entirely (Stahl, 2013). Antagonists, on the other hand, blocks the action of the agonist. There are four types of drug antagonism: chemical, physiological, pharmacokinetic, and pharmacologic. An example of chemical antagonism would be to use a different drug to block excess dopamine in the brain (Merck, 2018). A physiological antagonism occurs when two drugs have different actions at the same receptor, and they tend to cancel each other out (Merck, 2018). A pharmacokinetic antagonist is how the body reacts to drugs, how the drugs are absorbed, distributed, metabolized, and excreted by the body (Stahl, 2013). Pharmacologic antagonism occurs when the action of a full or partial agonist is inhibited in the pathway or at the receptor (Merck, 2018). Examples of antagonist drugs are naltrexone and naloxone, as they can attach to the opioids receptors without activating them, thereby blocking opioid’s effect (NIDA, 2018). The agonist-to-antagonist spectrum of the action of psychopharmacology either potentiates or diminishes the activity of neurotransmitters. The antagonist competes for a binding site, which might lessen the biological response to patients (Stahl, 2013). Compare and contrast the actions of G couple proteins and Ion gated channels. A G couple protein is known as an integrated membranes protein which converts extracellular signals into intracellular response, and serve as a target for drugs, especially psychotropic drugs (Miao, & McCammon, 2016). G couple protein plays a role in signal transduction and membrane vesicle transport and serves as targets for one-third of drugs that treat many human illnesses (Miao, & McCammon, 2016). On the other hand, Ion gated channels are known to regulate synaptic neurotransmission. Ion gated channels are stimulated when the gates open and close. Ion gated channels are made up of transmembrane proteins that create a channel in the cell membrane, allowing chemicals or charged ions to pass through an impermeable membrane (Huettner, 2013). G couple protein and Ion gated channel both have active sites for agonist binding. The binding of an agonist to an Ion gated channel receptor site allows ions like potassium and sodium to pass through, creating an electric signal (Stahl, 2013). G couple proteins and Ion gated channels are both transmembrane receptors. They are essential for the binding, transmitting, and activation of psychotropic agents, allowing these drugs to impact brain chemicals and neurotransmitters (Stahl, 2013). Explain the role of epigenetics in pharmacologic action. Epigenetics is the study of changes that occur in the genes without causing any change to the order of the DNA (Brown, 2020). Epigenetics is responsible for deciding whether a gene is expressed or not. For this to happen, the structure of the chromatin must be modified (Stahl, 2013). Epigenetic regulation of gene activity is vital in maintaining cells’ regular activity and has a role in the development of diseases (Stefanska, 2015). Chronic stress, drug abuse, and other environmental stimuli can trigger the epigenetic mechanisms leading to such modifications (Boks et al., 2011). Several lifestyle factors can modify epigenetic patterns. These include diet, obesity, physical activity, smoking, stress, and environmental pollutants. It is also theorized that epigenetic mechanisms can be utilized to treat addictions, extinguish fear, and prevent chronic pain. It may identify high-risk individuals and help prevent the disorder (Stahl, 2013). How this information will impact my practice Providers must know the action of agonists and antagonists’ agents. Understanding epigenetics is essential when studying treatment and prevention. It is the responsibility of the provider to understand the various factors, which include gender, age, and ethnicity, and how they can affect psychotropic medications and its mechanism of actions (Kusumi, Boku, & Takahashi, 2015). For example, a patient with bipolar disorder came to the hospital with increased mania, reported a reduced need for sleep and agitation. The patient has been taking Zoloft for depression by reviewing the patient’s medication records. Zoloft is a selective serotonin reuptake inhibitor (SSRI) (Nall, 2019). In clients with bipolar disorder, SSRI can increase mania symptoms and reduce the need for sleep and agitation (Nall, 2019). Instead of adding an SSRI to his medication, it would have been better to adjust his mood stabilizer medication to avoid the new symptoms. Understanding the specific mechanisms of SSRI’s and mood stabilizers would have prevented the provider from prescribing the client SSRI and therefore preventing adverse symptoms. References Boks, Marco P., Jong, Noelle M., Jong, Martien, Kas, Christiann, Vinkers, Cathy, Fernandes, Rene, & Kahn, S. (2011). Current status and future prospects for epigenetic psychopharmacology. Retrieved from https://www.tandfonline.com/doi/full/10.4161/epi.7.1.18688 Brown, J. (2020). What is epigenetics? Retrieved from https://www.ausmed.com/cpd/articles/what-is-epigenetics Huettner, J. (2013). Ion channel. Retrieved from https://www.britannica.com/science/ion-channel Kusumi, I., Boku, S., & Takahashi, Y. (2015). Psychopharmacology of atypical antipsychotic drugs: From the receptor binding profile to neuroprotection and neurogenesis. Psychiatry and clinical neurosciences, 69(5), 243-258. Merck & Co., Inc. (2018). Drug action and pharmacodynamics. Retrieved August 24, 2018 from https://www.merckvetmanual.com/pharmacology/pharmacology-introduction/drug-action-and-pharmacodynamics#v3329184 Miao, Y. & McCammon, J. (2016). G-Protein Coupled Receptors: Advances in Simulation and Drug Discovery. Retrieved on February 26, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5154880/ Nall, R. (2019). Antidepressants and Bipolar Disorder. Retrieved from https://www.healthline.com/health/bipolar-disorder/guide-antidepressants National Institute of Drug Abuse (NIDA) (2018). Opioids Agonist and Partial Agonists. (Maintenance Medications). Retrieved from, https://www.drugabuse.gov/publications/research-reports/medications-to-treat-opioid-addiction/how-do-medications-to-treat-opioid-addiction-work Rogers, K. (2019). G. protein-coupled receptor. Retrieved from https://www.britannica.com/science/G-protein-coupled-receptor Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press Stefanska, B. (2015). Epigenetics and pharmacology. British Journal of Pharmacology, 172(11), 2701-2704. https://doi.org/10.1111/bph.13136 Jamals post According to Zimmer (2016) when prescribing psychopharmacologic agents to a client, the medication can either increase or decrease the activity at the synapse. When there is increased activity at the synapse, it is identified as an agonist. However, when there is decreased activity it is called an antagonist. With that in mind, it is easier to see the complexity of psychopharmacological agents when it includes the agonist-to antagonist- spectrum of action. For example, antidepressants such as selective serotonin reuptake inhibitors (SSRI), hinder certain serotonin receptors within the brain. This stops the uptake of neurotransmitters through certain specific receptors (antagonist) while improving (agonist) concentration levels of other neurotransmitters within the brain (Grinde and Hendrick-Davis, 2017). Actions of g-couple proteins and ion gated channels are similar in the fact that both can mediate post synaptic synopsis or responses and are located within the membrane. The differences between the two is that the response derived from g couple proteins is rapid and use protein kinase when binding to molecules responsible in signaling, activating the g-protein. Ion gated channels are slower and orchestrate the flow of ions between the cell membrane. This slower process of ion channel linked receptors can open channels through the membrane, allowing specific ions to pass (Yudin and Rohacs, 2019). According to Cascorbi and Schwab (2016), the role of epigenetics in pharmacological action can either activate, deactivate, or perfect genetic enterprise. Epigenetics can impact drug metabolism and how the agent is transported throughout the human body. This information can impact how a psychiatric mental health nurse practitioner prescribes medications, by first forcing the provider to justify why certain psychopharmacological agents should be prescribed. This knowledge can help practitioners understand if the medication is better suited as a short term or long-term solution. Also, before prescribing there must be an understanding that when altering the functionality of certain neurotransmitters, potential side effects can occur. Examples are insomnia, nervousness, agitation, restlessness, and alteration in sexual functionality. Placing emphasis on a client centered approach can help promote medication compliance and improve the client’s mental health status. A situation relative to this is a client that is prescribed benzodiazepines due to a chronic history of anxiety. As the client continues the medication regimen, there is an increased risk of tolerance development. The practitioner continues to increase the dosage, but the client now suffers from the side effects such as increased drowsiness, dizziness, confusion, and impaired coordination. The client’s prescription of the medication was stopped which lead to withdrawal, placing the client at risk of developing severe anxiety, tremors and even seizures. By being aware of the medication’s actions the practitioner can understand that certain benzodiazepines are more suited as a short-term solution to the client’s anxiety issues. The need for a more long-term medication is needed such as Effexor XR, as the dosage can be minimal with a more longstanding in effectiveness. References Angell, B., & Bolden, G. B. (2015). Justifying medication decisions in mental health care: Psychiatrists’ accounts for treatment recommendations. Social science & medicine (1982), 138, 44–56. https://doi.org/10.1016/j.socscimed.2015.04.029 Cascorbi, I., & Schwab, M. (2016). Epigenetics in Drug Response. Clinical Pharmacology & Therapeutics, 99(5), 468-470. doi:10.1002/cpt.349 Grinde, E., & Herrick-Davis, K. (2017). Class A GPCR: Serotonin Receptors. G-Protein-Coupled Receptor Dimers, 129-172. doi:10.1007/978-3-319-60174-8_6 Yudin, Y., & Rohacs, T. (2019). The G‐protein‐biased agents PZM21 and TRV130 are partial agonists of μ‐opioid receptor‐mediated signalling to ion channels. British Journal of Pharmacology. doi:10.1111/bph.14702 Zimmer L. (2016). Pharmacological agonists for more-targeted CNS radio-pharmaceuticals. Oncotarget, 7(49), 80111–80112. https://doi.org/10.18632/oncotarget.13418