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27 Nov
2019

Agonist-to-Antagonist Spectrum Explained – NO PLAGIARISM

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Agonist-to-Antagonist Spectrum Explained
The concept of the agonist spectrum is that a full-agonists can produce a conformational change within a G-protein that causes the second messenger to be turned on to the greatest extent (Stahl, 2013). Additionally, full agonists produce full receptor activation, which produces maximum signal transduction (Stahl, 2013). Partial agonists stimulate receptors to a lesser degree than full agonists (Stahl, 2013).
The concept of antagonist is blocking the action of a neurotransmitter (Stahl, 2013). Antagonists can block the action of the agonist which produces conformation change within a G-protein that causes no signal transduction change (Stahl, 2013). Thus, the antagonist returns the G-protein conformation to the same state when the agonist was not present (Stahl, 2013). Additionally, since antagonists have no action of their own, they are considered “neutral” or “silent” (Stahl, 2013).
Some antagonists are inverse agonists. Inverse agonists are the opposite of agonists as they produce a conformational state of the receptor that causes inactivation and removes the low level of activity (i.e. constitutive activity) (Stahl, 2013). However, an antagonist can reverse an inverse antagonist by reversing the conformational state of the receptor that causes inactivation and allow constitutive activity (Stahl, 2013).
Action of G Couple Proteins and Ion Gated Channels
The action of G-proteins begins with a neurotransmitter binding to its receptor (Stahl, 2013). The mechanism causes the receptor to change to bind to the G-protein (Stahl, 2013). Then, the G-protein binds to the new conformation of the receptor-neurotransmitter complex (Stahl, 2013). Next, the neurotransmitter and the G-protein work together to allow the G-protein to bind to another enzyme and synthesize the second messenger within the inner membrane of the cell (Stahl, 2013). Thus, the enzyme, such as adenylate cyclase, binds to the G-protein to synthesize the second messenger, cyclic adenosine monophosphate (cAMP) (Stahl, 2013). The second messenger triggers the third chemical messenger to activate, kinases which add a phosphate group to proteins (Stahl, 2013). The action of kinases triggers the fourth chemical messenger to create phosphoproteins (Stahl, 2013).
Ion gated channels are essential in the signaling of the nervous system because they allow rapid and direct conversion of a neurotransmitter to an electrical current (Li, Wong, & Liu, 2014). There are several types of ion linked channels, such as ligand-gated ion channels and voltage-gated ion channels. Like the G-protein, ion channels are triggered by a neurotransmitter (Stahl, 2013). For instance, a first messenger neurotransmitter opens the ion channel to allow calcium to enter the neuron (Stahl, 2013). Calcium acts as the second messenger, which activates a different third messenger, known as phosphatase (Stahl, 2013). Unlike G-proteins, phosphatase removes the phosphate group from the fourth messenger phosphoprotein (Stahl, 2013). This action reverses the action of the third messenger. Thus, kinase and phosphatase activity, and the two neurotransmitters involved determine the chemical activity that activates the fourth messenger to trigger gene expression or synaptogenesis (Stahl, 2013).
The Role of Epigenetics in Pharmacological Action
Genetics is the deoxyribonucleic acid (DNA) code that a cell transcribes into specific types of ribonucleic acid (RNA) or translate into proteins (Stahl, 2013). Thus, epigenetics is a parallel system that determines if a gene is made into a specific RNA and protein or if the gene is ignored or silenced (Stahl, 2013). Epigenetics can modify the structure of chromatin within the cell to turn genes on or off and allows the gene to be read (expressed) or not read (silenced) (Stahl, 2013).
Epigenetics can play a role in pharmacological action by changing epigenomic patterns in mature cells through an enzyme called histone deacetylases (HDACs) (Stahl, 2013). HDACs silences the gene, and through demethylation and acetylation, the once silenced gene is reactivated (Stahl, 2013). For instance, epigenetic patterns like serotonin transporter methylation status can predict antidepressant pharmacotherapy responses ((Schuebel, Gitik, Domschke, & Goldman, 2016). Thus, epigenetic changes can predict disease response and can be useful as biomarkers to diagnose the progression of a disease (Schubel et al., 2016). Therefore, epigenetic plasticity can be a key mechanism for therapeutic interventions in mental disorders, and epigenetic changes can be biomarkers for lasting therapeutic effects, which can provide better predictions of treatment successes (Schubel et al., 2016).
How Information Impacts the Way Medications are Prescribed
As a prescriber, it is essential to know how medications work within the body. Understanding how the drug works helps providers know if the drug will be effective. It will also help decrease medication errors and potentially harmful situations. For instance, depression is a common disease worldwide (Dusi, Barlati, Vita, & Brambilla, 2015). Some clients will have symptoms that are benign, while other clients will have recurrent remitting episodes of depression (Dusi et al., 2015). Thus, it is essential for the psychiatric mental health nurse practitioner (PMHNP) to know how antidepressants work within the brain to understand the proper medication for the client.
A specific example would be a twenty-two-year-old female presenting herself in the office with symptoms of anxiety, hopelessness, loss of interest in activities, agitation, and mood swings. She is diagnosed with major depressive disorder (MDD). In major depression, it is thought that there are low levels of serotonin. Thus, it is common to prescribe a selective serotonin reuptake inhibitor (SSRI) to patients with MDD. The PMHNP needs to understand that SSRIs block the reuptake of serotonin at the synaptic cleft, which helps relieve the symptoms of depression.
Reference
Dusi, N., Barlati, S., Vita, A., & Brambilla, P. (2015). Brain structural effects of antidepressant treatment in major depression. Current Neuropharmacology, 13(4), 458-465. doi: 10.2174/1570159X1304150831121909
Li, S., Wong, A.H.C., Liu, F. (2014). Ligand-gated ion channel interacting proteins and their role in neuroprotection. Frontiers in Cellular Neuroscience. Retrieved from https://doi-org.ezp.waldenulibrary.org/10.3389/fncel.2014.00125
Schuebel, K., Gitik, M., Domschke, K., & Goldman, D. (2016). Making sense of epigenetics. International Journal of Neuropsychopharmacology, 19(11). Retrieved from https://doi.org/10.1093/ijnp/pyw058
Stahl, S.M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical application (4th ed). New York, NY: Cambridge University Press.

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