Assignment: Agonist-to-antagonist spectrum of action Assignment: Agonist-to-antagonist spectrum of action Analyze the agonist-to-antagonist spectrum of action of psychopharmacologic agents APA Format, 3 credible references, not more than 5 years old, No certain length, Just make sure to answer the question the instrctor is asking. Post a response to each of the following: Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents. Compare and contrast the actions of g couple proteins and ion gated channels. Explain the role of epigenetics in pharmacologic action. Explain how this information may impact the way you prescribe medications to clients. Include a specific example of a situation or case with a client in which the psychiatric mental health nurse practitioner must be aware of the medications action. Discussion: Foundational Neuroscience As a psychiatric mental health nurse practitioner, it is essential for you to have a strong background in foundational neuroscience. In order to diagnose and treat clients, you must not only understand the pathophysiology of psychiatric disorders, but also how medications for these disorders impact the central nervous system. These concepts of foundational neuroscience can be challenging to understand. Therefore, this Discussion is designed to encourage you to think through these concepts, develop a rationale for your thinking, and deepen your understanding by interacting with your colleagues. ORDER YOUR PROFESSIONAL PAPER HERE Learning Objectives Students will: Analyze the agonist-to-antagonist spectrum of action of psychopharmacologic agents Compare the actions of g couple proteins to ion gated channels Analyze the role of epigenetics in pharmacologic action Analyze the impact of foundational neuroscience on the prescription of medications Learning Resources Note: To access this weeks required library resources, please click on the link to the Course Readings List, found in theCourse Materials section of your Syllabus. Required Readings ? Assignment: Agonist-to-antagonist spectrum of action Note: All Stahl resources can be accessed through the Walden Library using this link. This link will take you to a log-in page for the Walden Library. Once you log into the library, the Stahl website will appear. Stahl, S. M. (2013). Stahls essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press *Preface, pp. ix?x Note: To access the following chapters, click on the Essential Psychopharmacology, 4th ed tab on the Stahl Online website and select the appropriate chapter. Be sure to read all sections on the left navigation bar for each chapter. Chapter 1, ?Chemical Neurotransmission? Chapter 2, ?Transporters, Receptors, and Enzymes as Targets of Psychopharmacologic Drug Action? Chapter 3, ?Ion Channels as Targets of Psychopharmacologic Drug Action? Assignment: Agonist-to-antagonist spectrum of action Order Now

ADDITIONAL INFORMATION 

Agonist-to-antagonist spectrum of action

Introduction

Agonists are molecules that bind to receptors. Agonists can have a variety of effects on target cells, but they all share the common property of causing an increase in cellular activity when bound to their respective receptors. Antagonists, on the other hand, bind to receptors and cause inhibition of the biochemical processes that happen when those receptors are activated by agonists. In other words, antagonists are inverse agonists – they bind to receptors, inhibit their activation and activate other downstream targets (such as transcription factors). Different types of chemical compounds can fit either side of this spectrum: some compounds act as full-strength agonists while others act as partial ones or inverse ones.

The antagonist-to-agonist spectrum of activity

Antagonists can be competitive, uncompetitive or non-competitive.

The competitive antagonist binds to the receptor and blocks the agonist from binding. For example, theophylline competes with and blocks caffeine in your bloodstream. In contrast, an uncompetitive antagonist doesn’t bind to any receptors—it simply stops their activity altogether.

Definition

An antagonist is a compound that binds to the same receptors as its agonist, but with less affinity. An example of this would be an anticholinergic drug like atropine. When used in low doses, the anticholinergic agent will bind to acetylcholine receptors and inhibit their activity, thereby decreasing arousal or excitement caused by stimulation of these receptor sites. However, if you take large quantities of atropine (e.g., more than 10 milligrams per dose), then it will also block muscarinic acetylcholine receptors (M3), which are responsible for constriction of smooth muscles such as those in your bronchi; this causes constriction symptoms when inhaled into your lungs during exercise or coughing—the opposite effect from what happens when using an anticholinergic agent!

Agonism vs. antagonism

Agonist and antagonist are two important concepts in pharmacology, which is the study of drugs (both natural and synthetic) that affect how a body responds to external stimuli.

An agonist is a compound that binds to a receptor on cell membranes, triggering a response from those receptors. The body produces chemicals called neurotransmitters when it’s stimulated by these agonists; these neurotransmitters then cause other cells and tissues in your body to do something—like swell up or contract—that helps you feel better.

Antagonists block the effects of agonists by binding at particular sites on these membranes so that they can’t trigger any kind of response with their action potentials (signals sent between neurons). Antagonists work similarly to antiseptics: they kill bacteria by stopping them from living long enough for them to multiply into harmful colonies; however unlike antiseptics which work only against specific types of bacteria while being harmless themselves this way…

Receptor selectivity and functional selectivity

Receptor selectivity is the ability of a drug to bind to a specific receptor subtype. Receptor selectivity and functional selectivity are not always correlated, but they often occur together. For example, dopamine agonists such as levodopa can produce both motor and cognitive side effects (functional side effects) while antagonists like ketamine produce only motor side effects like hallucinations and euphoria.

Allosteric modulators

Allosteric modulators are a type of drug that binds to a protein and changes its shape, but does not activate or inhibit the protein. Allosteric modulators have been shown to have significant effects on both positive and negative allosteric sites. By binding at allosteric sites, these drugs can increase or decrease their effect on a given target molecule (i.e., receptor). Allosteric modulators can be either positive or negative in nature; this means they will bind to either an agonist-binding site or an antagonist-binding site but not both types of binding sites at once; this leads us back into our discussion about how drugs interact with proteins: if one side of your molecule is bound by something else then that other thing will block access from using its own chemical structure as well as blocking access from using another part of your body’s chemistry through which you might want access – like when I’m trying out my new perfume while walking around town until my friend comes over after work so we could go out together tonight!

Positive allosterics modulators (PAMs)

Positive allosteric modulators (PAMs) are compounds that bind to the same receptor as an agonist, but they do not activate the receptor. In this way, they increase the activity of a protein by increasing its affinity for that agonist.

Some examples of PAMs include:

• Phosphodiesterase inhibitors – These are used to treat erectile dysfunction and premature ejaculation in men, among other conditions

Negative allosteric modulators (NAMs)

NAMs are compounds that bind to the same site as agonists but do not activate the receptor. The binding of a NAM to its target is reversible, meaning it can be displaced by an agonist or antagonist.

NAMs may act either as competitive antagonists or non-competitive antagonists; however, in both cases there is a difference between how they affect the affinity for G protein activation and phosphodiester bond formation. In competitive antagonists, binding induces dissociation of an allosteric modulator from its target molecule (i), which leads to a decrease in free energy compared with non-competitive antagonists (ii).

Partial agonists

Partial agonists are drugs that bind to the receptor and produce a partial response. For example, adrenaline is a full agonist of the adrenergic receptor, but it’s also an extremely potent partial agonist for other targets too; this allows you to use less of it by selectively targeting specific receptors.

Partial agonists are often used in disease areas where there is overactive signaling at one or more sites on the body (e.g., heart disease). When used as a treatment for these diseases, they can help restore homeostasis by reducing activation of certain pathways while increasing others.

Inverse agonists

Inverse agonists are drugs that bind to the same receptor as an agonist, but do not elicit the same response.

• Full inverse agonists: These drugs are fully effective at antagonizing effects of full agonists. For example, if you take a drug that’s known to have antidepressant properties and it fails to produce its intended effect (for example, if you don’t feel better after taking antidepressants), then your doctor may prescribe a full inverse agonist instead of another antidepressant medication because it may work just as well for you.

• Partial inverse agonists: Partial inverse agonists reduce some of the adverse effects associated with full antagonists (for example: sedation or nausea), but they also induce some unwanted side effects such as cardiovascular depression or sexual dysfunction due to central nervous system depression; therefore they are best reserved for cases where these undesirable side effects outweigh any potential benefit gained from using them over traditional antidepressants such as SSRIs ( serotonin reuptake inhibitor) which have few adverse reactions versus SSRI-like drugs (antidepressants).

Conclusion

These compounds have a strong affinity for the receptor and have little affinity for other receptors, but they do not activate some of the physiological functions of other ligands. In contrast, inverse agonists bind to allosteric sites on the G protein-coupled receptor to inhibit or block its interaction with the heterotrimeric G protein–GTP complex. This prevents activation of downstream signaling molecules such as adenylyl cyclase or phospholipase C. Inverse agonists are used in many areas of medicine because they can be used to treat conditions where activation would be undesirable (e.g., pain) while remaining relatively safe at low doses.

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