20 Mar Agonist-to-antagonist spectrum of action of psychopharmacologic agents.
Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents.
To comprehend the agonist-to-antagonist spectrum of action of psychopharmacologic agents, it is vital to know that an agonist is a chemical that binds to a receptor, and when the receptor activates, an organic response is produced. In contrast, an antagonist blocks the action of agonist, and an inverse agonist causes an action opposite to that of the agonist (Stahl, S.M., 2013). The agonist spectrum can be classified into four types. A full agonist is generally represented by the natural neurotransmitter itself. Some drugs can act as natural neurotransmitters (Stahl, 2013). The receptor ligands that bind to certain receptors in order to produce the desired therapeutic effect. Specifically, agonists bind to receptors and modulate the activation of the receptors in order to produce the requisite action (Stahl, 2013). The agonist opens the channel the maximal amount and frequency allowed by the binding site, while antagonists that lie in the middle of the spectrum retain the resting state with the infrequent opening of the channel. The inverse agonist placed the ion channel into a closed and inactive state. Antagonists hold the ability to block anything in the agonist spectrum, and ions are returned to their resting state in each instance (Stahl, 2013). An agonist tie to a receptor site and causes a response while an antagonist works against the drug and blocks the receptor. An agonist stimulates the action, while the antagonist sits idle, doing nothing. Since there is no difference between the presence and absence of the antagonist, the antagonist is said to be neutral or silent (Stahl, 2013).
Compare and contrast the actions of g couple proteins and ion gated channels.
To fully appreciate the action of ion gated channels, one must understand the two comprehensive receptor proteins. Their action is completed by opening and closing postsynaptic ion channels. The receptor in one of these receptors is called the ionotropic receptor which is linked straight to ion gated channels (Stahl, 2013). These receptors perform a dual purpose; an extracellular site binds the neurotransmitters, and the membrane-spanning area forms an ion channel. As a result, inotropic receptors combine transmitter-binding and channel functions into one molecular unit called ligand-gated ion channels (Stahl, 2013).
The other neurotransmitter is the metabotropic receptor, also referred to as G-protein-coupled receptors (Stahl, 2013), which controls the movement of ion depending on multiple metabolic steps. There are no ion channels, but channels are affected by the activation of intermediate molecules called G-protein. Metabotropic receptors are monomeric proteins having an extracellular area for neurotransmitter binding and an intracellular area for binding to G-proteins (Stahl, 2013).
Explain the role of epigenetics in pharmacologic action,
Epigenetic mechanisms have played an essential role in modulating these properties by regulating gene expression. Epigenetic regulation of gene activity has been shown to be important in maintaining the normal phenotypic activity of cells, as well as having a role in development and diseases such as neurodegenerative disorders such as Alzheimer’s (Stefanska & MacEwan,2015). Original classes of drugs regulate epigenetic mechanisms to counteract disease states in humans, however, these drugs may not be designed to be as precise to a particular ligand or specific to a particular gene or protein subtype, they may indeed have to be able to be more broad-acting over a range of large-scale epigenetic events (Narayan & Dragunow,2015). Epigenetic regulates the gene activity; this is important to maintain the normal phenotypic activity of cells as well as having a role in development and diseases such as cancer and neurodegenerative disorders such as Alzheimer’s. The epigenetic mechanism turns genes on and off by modifying the structure of chromatin in the cell nucleus (Stahl, S. M. (2013). With recent improvements in understanding of the actual function of the entire genome, pharmacology must modify itself further to think of tackling diseases, not in the conventional drug-receptor sense, but in a more global-response sense.
Analyze the impact of foundational neuroscience on the prescription of medications.
It is no secret that when you get older your body does not work the way it used to, and that is true for how you react to the medicine. Aging is characterized by a deterioration in the maintenance of homeostatic processes over time, leading to functional decline and increased risk for disease and death (Barzilai, Huffman, Muzumdar & Bartke, 2015). When dealing with the brain and prescription medication the clinician needs to understand how the drug works in the body as well as the brain. Grouping psychotropic medications as indicated by impacts on mental capacities is important to consider as Practitioners. There is a strong need for this so that the patient is receiving the right medications and had a maximum benefit and positive reaction prescribed medication (Barzilai et al, 2015). The clinician should also understand the interactions with other medications the patient may be taking and any allergies. Psych drugs have many interactions and will react differently in the brain if not taken correctly.
Reference
Barzilai, N., Huffman, D. M., Muzumdar, R. H., & Bartke, A. (2015). The critical role of metabolic pathways in aging. Diabetes, 61(6), 1315-22. Retrieved from https://search-proquest-com.ezp.waldenulibrary.org/docview/1022340571?accountid=14872
Narayan, P., & Dragunow, M. (2015). Pharmacology of epigenetics in brain disorders. British
journal of pharmacology, 159(2), 285–303. doi:10.1111/j.1476-5381.2009.00526.x
Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University.
Stefanska, B., & MacEwan, D. J. (2015). Epigenetics and pharmacology. British journal of pharmacology, 172(11), 2701–2704. doi:10.1111/bph.13136
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