NUR 6630 Week 1 Discussion: Foundational Neuroscience

NUR 6630 Week 1 Discussion: Foundational Neuroscience
Explain the agonist-to-antagonist spectrum of action of .
Full agonists allow a receptor site to open up an ion channel to the maximum amount and frequency which is allowed by that particular binding site which causes the maximum amount of downstream signal transduction to be utilized at the binding site. The ion channel can open more frequently than with a full agonist alone but requires the help of a second receptor site. An antagonist causes a stabilization in the receptor sites in resting phases which is the same mechanism of action at the receptor site when an agonist is not present. Because there are no changes whether an antagonist is present or not, it is said to be neutral or silent.
NUR 6630 Week 1 Discussion Foundational Neuroscience
In response to partial agonists, receptors modify in a way that causes ion channels to open more frequently and to a greater extent than they would in a resting state, but not as frequently as they would in the presence of a full agonist. As with full agonists, antagonists counteract partial antagonists and return the receptor site to its resting state. Partial agonists increase ion flow and downstream signal transduction, but not to the extent of a full agonist, compared to the resting state. The receptor output must be balanced to prevent too much or too little downstream action from occurring when there are unstable neurotransmissions within the brain. Stabilizers are another name for partial agonists, which have the ability to maintain a steady response between the extremes of an excessive or insufficient action potential (Stahl, 2013).
Compare and contrast the actions of g couple proteins and ion gated channels.
A class of receptors linked to G proteins are a major target of psychotropic drugs. The G couple proteins have the structure of seven transmembrane regions, spanning the membrane seven times. Each region of the membrane is arranged around a central core which contains a binding site for a neurotransmitter. Drugs can interact at a particular neurotransmitter binding site or at other sites, also called allosteric sites within a receptor. This binding can lead to various modifications of receptor actions by either partially or fully mimicking or blocking any neurotransmitter function which would normally occur at a specific receptor site. Downstream molecular processes can be changed by drug actions as when phosphoproteins are activated or inactivated which results in a difference in which enzymes, receptors, or ion channels are modified by the neurotransmission. These drug actions can also lead to changes in which genes are expressed, altering which proteins are synthesized and which functions are amplified, from synaptogenesis, to receptor and enzyme synthesis, to communication with downstream neurons innervated by the neuron with the G-protein-linked receptor. As a result, drug-induced alterations at the G-protein-linked receptor site can cause actions on psychiatric disorders or symptoms (Stahl, 2013).
Like G proteins, ligand-gated ion channels are a type of receptor which also forms an ion channel. For this reason, they are both ligand-gated ion channel and also ionotropic receptors or ion-channel-linked receptors. They have dual functions, hence the two names. Ligand-gated ion channels consist of long strings of amino acids which are gathered as subunits around an ion channel. There are many binding sites around these subunits for , ions and drugs. Complex proteins have sites where ions can pass through a channel or bind to the channel, or where a neurotransmitter can act as a binding site and where natural substances or drugs can bind to a site different than where the neurotransmitter binds resulting in an increase or decrease to the sensitivity of a channel opening. In psychopharmacology, the ion channels that are the most important are those that control sodium, calcium, chloride, and potassium. Full agonists will directly change the receptor site to open the ion channel. Antagonists will cause a steady state at the receptor in its resting state which is similar to how a receptor responds when there is no agonist present. Alternatively, drug-induced modifications which occur with ionotropic receptors cause immediate effects by changing the flow of ions resulting in an immediate clinical onset as when medications such as anxiolytics and hypnotics are used. Some drugs that act at the G-protein-linked receptor sites may have a delayed response caused by an instigation in cellular functions that become activated by the signal transduction cascade (Stahl, 2013).
Explain the role of epigenetics in pharmacologic action.
RNA and proteins are transcribed from an unique DNA sequence within cells. Humans have more than 20,000 genes, however not all of them are expressed in the brain. While genetics can explain how a gene is expressed as a particular RNA or protein, epigenetics goes one step further by determining if the gene itself is actually expressed. The epigenome, on the other hand, is defined as the “narrative” of all the “words” in the genome that come together to form a cohesive whole. Every neuron and cell in the body has the same genetic make-up as potential proteins. How a neuron becomes a neuron, for example, or how it becomes a liver cell instead of a neuron, depends on whether or not specific genes are activated or silenced. Mental problems can result if genes with aberrant sequences are expressed rather than silenced in neurons that are malfunctioning. If faulty genes are expressed and/or normal genes are repressed, the development of the brain will be affected. , genetic make-up, medicines, and the environment are just a few of the things that play a role in determining whether or not genes are expressed or repressed. A person’s drug usage, stress, and other mental health issues all influence into whether or not medicine and counseling will help them better their condition (Stahl, 2013).
Explain how this knowledge may affect your prescriptions for patients. The psychiatric mental health nurse practitioner must be knowledgeable of the medication’s action in a specific setting or case with a patient.
Prior to prescribing any medication, it is critical to have a thorough understanding of its pharmacodynamics, pharmacokinetics, and toxicology. In addition, one must be aware of genetics and factors that influence medicine absorption and uptake. From a social worker’s perspective, Farmer (2014) argues that a new understanding of mental illness is emerging. In an effort to rethink mental disorder diagnosis, the National Institute of Mental Health has worked on a project (the Research Domain Criteria RDoC). When it comes to studying mental disease, the RDoC makes use of data from the fields of genetics and neuroscience. An emphasis is being placed on investigating the biological underpinnings of mental diseases, and this includes a new knowledge of various aspects of functioning related to positive and negative valence systems, cognitive systems, systems for social activities, and arousal/modulatory systems. Additionally, client behavior and self-reports are taken into account. Mental disease diagnosis will be linked with neurobiology and better treatments will be discovered. It’s important to realize that psychotropic drugs function by altering the concentration of a neurotransmitter in the brain and central nervous system. Axons transmit chemical and electrical signals to receptive neurons, while synapses serve as a point of communication between neurons and the site of an action potential. This brain activity is the source of human behavior. It is important for us as PMHNPs to have an understanding of how a medicine works and how it affects the primary neurotransmitters (acetylcholine and norepinephrine) and how they are changed by specific medications. Medications affect patients in varied ways, depending on their age, gender, color, and ethnicity, for example. Racially and ethnically diverse populations may have different pharmacokinetic and pharmacodynamic profiles, which are impacted by genetic and environmental variables, including lifestyle, behavior, and social contact. In order for a medication to work for one person, it must be paired with their genes and their surroundings (Farmer, 2014).
Patients with mental health issues including major depressive disorder and drug addiction can benefit from understanding that numerous genes are involved rather than the “one gene and one disease” model. There is hope that better understanding of epigenetic modifications (such as acetylation and deacetylation of histones and DNA methylation) could lead to more effective treatments for mental health issues (Mahgoub & Monteggia, 2013).
When prescribing SSRIs or SNRIs, PMHNPs should keep in mind that these drugs require time to have a therapeutic impact. As a patient, you need to know that you won’t feel “well” right away, and you should be encouraged to stick with your medicine and therapy regimen.
References
Farmer, R. L. (2014). Interface between psychotropic medications, neurobiology, and mental illnesses. Smith College Studies in Social Work, 84(2-3), 255-272.
Mahgoub, M., & Monteggia, L. M. (2013). Epigenetics and psychiatry. Neurotherapeutics, 10, 734-741.
Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press.
To prepare for this Discussion:
Review this week’s Learning Resources.
Reflect on concepts of .
Note: For this Discussion, you are required to complete your initial post before you will be able to view and respond to your colleagues’ postings. Begin by clicking on the “Post to Discussion Question” link and then select “Create Thread” to complete your initial post. Remember, once you click on Submit, you cannot delete or edit your own posts, and you cannot post anonymously. Please check your post carefully before clicking on Submit!
By Day 3
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 medication’s action.
Read a selection of your colleagues’ responses.
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.
Week 1 discussion
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.
Learning Objectives
Students will:
Analyze the agonist-to-antagonist
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 week’s required library resources, please click on the link to the Course Readings List, found in the Course Materials section of your Syllabus.
Required Readings
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). Stahl’s 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 y, 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”
Document: Midterm Exam Study Guide (PDF)
Document: Final Exam Study Guide (PDF)
Required Media
Laureate Education (Producer). (2016i). Introduction to [Video file]. Baltimore, MD: Author.
Note: The approximate length of this media piece is 3 minutes.
Accessible player
Optional Resources
Laureate Education (Producer). (2009). Pathopharmacology: Disorders of the nervous system: Exploring the human brain [Video file]. Baltimore, MD: Author.
Note: The approximate length of this media piece is 15 minutes.
Dr. Myslinski reviews the structure and function of the human brain. Using human brains, he examines and illustrates the development of the brain and areas impacted by disorders associated with the brain.
Accessible player
Laureate Education (Producer). (2012). Introduction to advanced pharmacology [Video file]. Baltimore, MD: Author.
Note: The approximate length of this media piece is 8 minutes.
In this media presentation, Dr. Terry Buttaro, associate professor of practice at Simmons School of Nursing and Health Sciences, discusses the importance of pharmacology for the advanced practice nurse.
Accessible player
To prepare for this Discussion:
Review this week’s Learning Resources.
Reflect on concepts of .
Foundational Neuroscience
Question 1
The psychopharmacologic drug effects of medications are based on the spectrum of agonist to an antagonist. Agonists are molecules that mimic the specific impacts of biological neurotransmitters by binding to and stimulating the receptor sites to produce a response similar to that elicited by a biological molecule. An antagonist, on the other hand, blocks the actions of neurotransmitters. While these represent two extreme aspects of psychopharmacologic drug effects, the agonist spectrum to antagonist ranges from full agonists, partial agonists, silent antagonists, inverse agonists, and irreversible agonists. Full agonists generally lead to the full ion channel opening for maximal signal transduction (Huang et al., 2020).
On the other hand, partial agonists partially improve signal transduction and elicit responses that do not match the full agonist. Silent antagonists have the impact of returning receptors to their resting states. Inverse antagonists ideally surpass and antagonism and have the effect of blocking constitutive activity (Fuller et al., 2019). On the other hand, the irreversible agonists bind and activate receptors but do not activate the receptor. Given that their binding is permanent, they generally lead to receptor destruction. Therefore, the psychopharmacological action of a drug depends on the available position in the agonist to antagonist spectrum.
Question 2
G-coupled proteins are a family of membrane proteins activated by a spectrum of structurally diverse molecules. These molecules are made up of seven different protein units spanning the membrane up to seven-time. They serve to transmit signals after neurotransmitters bind to the receptors. Drug binding to the receptor sites leads to a partial or full blocking of the functions of the neurotransmitters. Ion-gated channels, on the other hand, are controlled electrically. Unlike ions, G-proteins can freely diffuse through the membrane and change their behaviors (Yudin, & Rohacs, 2019). Ions cannot freely pass through the membrane due to their presenting charges. Therefore, ions-gated channels control access into and out of the neurons. On the other hand, both the G-coupled proteins and the ion-gated channels are types of protein receptors. Therefore, the medications that alter the flow of ions can have a faster clinical effect, unlike the drugs targeting G-protein-linked sites that take a more extended period to produce an impact.
Question 3
Epigenetics refers to the study of how DNA interacts with smaller molecules that can deactivate or activate genes within the cells. Ideally, epigenetic changes form part of the typical development spectrum and influence multiple factors, including medications. The experienced epigenetic changes lead to disease states or the regulation of pre-existing disease states (Cavalli, & Heard, 2019). Therefore, drugs can target specific genes coding for enzymes, neurotransmitters, and other molecules responsible for a pathological state. This way, epigenetics can be applied in understanding the pharmacological aspects of a drug.
Question 4
To provide a prescription of drugs and monitor their effects on patients, PMHNPs must comprehend the mechanisms through which drugs act. Further, there is a need to evaluate the targeted outcome, the mechanical action of the drug, and the side effects of the medications. For instance, a drug like Clozapine is prescribed as an atypical antipsychotic for schizophrenia resistant to treatment (Caraci et al., 2017). Further, the medication has a risk associated with constipation, orthostatic hypotension, seizures, and myocarditis. Therefore, practitioners must understand the need for close monitoring due to their effect on white blood cells and the different dynamisms of practice in understanding drug action mechanisms.
Pharmacological agents produce both agonist and antagonist actions in different receptors in the human body. The agonist and antagonist actions of pharmacological agents work against one another. The agonists combine with the receptor to produce an action in the body. On the other hand, antagonist action hinders or opposes the action by a receptor, thereby, leading to a failure of an occurrence of an event. The effect of agonists is attributed to the combination it has with compounds or chemical substances to promote the desired action while that of antagonist entails the combination with chemicals or blockage of neurotransmitters to cause interference with action. Partial and inverse agonists have an effect on the efficacy of psychopharmacological agents. Partial agonists bind to a specific receptor to produce partial efficacy at that receptor that is relative to the effect of full agonist. The partial enhancement of the actions of the receptor results in a net decline in the activation of the receptor hence, average activity of the receptor in producing the desired action. Inverse agonists work by binding to a receptor as an antagonist to produce an action that is opposite to that of the agonist (Demler, 2019). Inverse agonists mimic the agonist activity of the receptors, hence, the desired therapeutic activity of psychopharmacological agents.
G-couple proteins and ion-gated channels are the mechanisms in which cells communicate to produce actions. They comprise of the cell-surface receptors that play the roles of signal transfer in multicellular organisms. The two however differ in a number of aspects. Ion-gated channels have receptors that bind to a ligand to cause opening of channels via membranes to allow the passage of specific ions. Ion-gated channels do not allow the passage of fatty acids and amino acids because they are hydrophobic in nature. Ion-gated channels therefore mediate rapid, post-synaptic responses. G-proteins channels on the other hand have receptors that bind and active G-protein on cell membranes. The activation of G-proteins results in cyclic series that cause entry of proteins such as amino acids and fatty acids into the cell to produce action (Hood & Khan, 2020). The G-proteins therefore mediate slow post-synaptic responses.
Rubric Detail
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Name: NURS_6630_Week2_Discussion_Rubric
Response to the Discussion question is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources.
40 (40%) – 44 (44%)
Thoroughly responds to the Discussion question(s).
Is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources.
No less than 75% of post has exceptional depth and breadth.
Supported by at least three current credible sources.
35 (35%) – 39 (39%)
Responds to most of the Discussion question(s).
Is somewhat reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module.
50% of the post has exceptional depth and breadth.
Supported by at least three credible references.
31 (31%) – 34 (34%)
Responds to some of the Discussion question(s).
One to two criteria are not addressed or are superficially addressed.
Is somewhat lacking reflection and critical analysis and synthesis.
Somewhat represents knowledge gained from the course readings for the module.
Post is cited with fewer than two credible references.
0 (0%) – 30 (30%)
Does not respond to the Discussion question(s).
Lacks depth or superficially addresses criteria.
Lacks reflection and critical analysis and synthesis.
Does not represent knowledge gained from the course readings for the module.
Contains only one or no credible references.
Main Posting:
Writing
6 (6%) – 6 (6%)
Written clearly and concisely.
Contains no grammatical or spelling errors.
Adheres to current APA manual writing rules and style.
5 (5%) – 5 (5%)
Written concisely.
May contain one to two grammatical or spelling errors.
Adheres to current APA manual writing rules and style.
4 (4%) – 4 (4%)
Written somewhat concisely.
May contain more than two spelling or grammatical errors.
Contains some APA formatting errors.
0 (0%) – 3 (3%)
Not written clearly or concisely.
Contains more than two spelling or grammatical errors.
Does not adhere to current APA manual writing rules and style.
Main Posting:
Timely and full participation
9 (9%) – 10 (10%)
Meets requirements for timely, full, and active participation.
Posts main Discussion by due date.
8 (8%) – 8 (8%)
Posts main Discussion by due date.
Meets requirements for full participation.
7 (7%) – 7 (7%)
Posts main Discussion by due date.
0 (0%) – 6 (6%)
Does not meet requirements for full participation.
Does not post main Discussion by due date.
First Response:
Post to colleague’s main post that is reflective and justified with credible sources.
9 (9%) – 9 (9%)
Response exhibits critical thinking and application to practice settings.
Responds to questions posed by faculty.
The use of scholarly sources to support ideas demonstrates synthesis and understanding of learning objectives.
8 (8%) – 8 (8%)
Response has some depth and may exhibit critical thinking or application to practice setting.
7 (7%) – 7 (7%)
Response is on topic, may have some depth.
0 (0%) – 6 (6%)
Response may not be on topic, lacks depth.
First Response:
Writing
6 (6%) – 6 (6%)
Communication is professional and respectful to colleagues.
Response to faculty questions are fully answered, if posed.
Provides clear, concise opinions and ideas that are supported by two or more credible sources.
Response is effectively written in Standard, Edited English.
5 (5%) – 5 (5%)
Communication is mostly professional and respectful to colleagues.
Response to faculty questions are mostly answered, if posed.
Provides opinions and ideas that are supported by few credible sources.
Response is written in Standard, Edited English.
4 (4%) – 4 (4%)
Response posed in the Discussion may lack effective professional communication.
Response to faculty questions are somewhat answered, if posed.
Few or no credible sources are cited.
0 (0%) – 3 (3%)
Responses posted in the Discussion lack effective communication.
Response to faculty questions are missing.
No credible sources are cited.
First Response:
Timely and full participation
5 (5%) – 5 (5%)
Meets requirements for timely, full, and active participation.
Posts by due date.
4 (4%) – 4 (4%)
Meets requirements for full participation.
Posts by due date.
3 (3%) – 3 (3%)
Posts by due date.
0 (0%) – 2 (2%)
Does not meet requirements for full participation.
Does not post by due date.
Second Response:
Post to colleague’s main post that is reflective and justified with credible sources.
9 (9%) – 9 (9%)
Response exhibits critical thinking and application to practice settings.
Responds to questions posed by faculty.
The use of scholarly sources to support ideas demonstrates synthesis and understanding of learning objectives.
8 (8%) – 8 (8%)
Response has some depth and may exhibit critical thinking or application to practice setting.
7 (7%) – 7 (7%)
Response is on topic, may have some depth.
0 (0%) – 6 (6%)
Response may not be on topic, lacks depth.
Second Response:
Writing
6 (6%) – 6 (6%)
Communication is professional and respectful to colleagues.
Response to faculty questions are fully answered, if posed.
Provides clear, concise opinions and ideas that are supported by two or more credible sources.
Response is effectively written in Standard, Edited English.
5 (5%) – 5 (5%)
Communication is mostly professional and respectful to colleagues.
Response to faculty questions are mostly answered, if posed.
Provides opinions and ideas that are supported by few credible sources.
Response is written in Standard, Edited English.
4 (4%) – 4 (4%)
Response posed in the Discussion may lack effective professional communication.
Response to faculty questions are somewhat answered, if posed.
Few or no credible sources are cited.
0 (0%) – 3 (3%)
Responses posted in the Discussion lack effective communication.
Response to faculty questions are missing.
No credible sources are cited.
Second Response:
Timely and full participation
5 (5%) – 5 (5%)
Meets requirements for timely, full, and active participation.
Posts by due date.
4 (4%) – 4 (4%)
Meets requirements for full participation.
Posts by due date.
3 (3%) – 3 (3%)
Posts by due date.
0 (0%) – 2 (2%)
Does not meet requirements for full participation.
Does not post by due date.
Total Points: 100
Name: NURS_6630_Week2_Discussion_Rubric
Agonist-to-Antagonist Spectrum of Action of Psychopharmacologic Agents
Communication between neurotransmitters is vital to the human body functions. Adding psychopharmacologic drugs to treat disease act to mimic the action of responsibility of neurotransmitters. “An agonist binds to a receptor and the receptor is activated, signal transduction occurs, and the outcome is a biological response. An antagonist binds to a receptor and blocks the receptor for binding by any agonists. There is no biological response” (Yeng-Tseng & Yang-Hsiang, 2017). Partial agonist or low efficacy agonist function is to partially produce a response. Psychopharmacologic treatment using an inverse agonist act as a negative intrinsic efficacy. From research, it is not yet understood from the writer in a clear, simplex way from the cellular level how agonist to antagonist is in relations. It is understood that agonist and antagonist that are used to treat psychiatric such as schizophrenia and Parkinson’s can be controlled with a dopamine antagonist. “Antagonists generally prove to be better electron acceptors and worse electron donors than dopamine, whereas agonists present an electron donor-acceptor capacity similar to that of dopamine” (Martinez, 2019).
Compare and Contrast the actions of G couple proteins and ion gated channels
It is understood that G coupled protein assists cells to convert signals outside the cell into intracellular response regulating physiology functions. “G protein–coupled receptors (GPCRs) mediate the majority of cellular responses to external stimuli, including light, odors, hormones, and growth factors” (Weis & Kobilka, 2018). Ion gated channels form proteins that are pores and can be thought of as a door that would allow the flow of ions across the membrane that may or may not be gated with voltage. It assists in binding neurotransmitters for a response. Ion gated channels and G coupled protein interact with each other to promote function of the nervous system.
Epigenetics Role
The regulation of gene expression through alterations of DNA has become an evolution to control disease. Although epigenetics changes are reversible by changing the way your body reads DNA sequences, it does not change DNA for good. “Epigenetic mechanisms, known for their ability to regulate gene transcription and genomic stability, are key players for maintaining normal cell growth, development, and differentiation” (Mazzone et al., 2019). Using pharmaceutical treat through epigenetics can help treat disease based on DNA factors.
Prescribing Medications to Patient
As a clinician, using the information describe above impacts prescribing as two patients may have the same disease but genetic factors may play a role in response in a negative or positive way. Assessing the patient thoroughly including environmental factors and genetics is essential for best outcomes. For example, treatment for depression may impact the patient’s cardiovascular system based on the action. “Serotonin–norepinephrine reuptake inhibitors, particularly venlafaxine, carry a greater risk of hypertension, possibly related to greater effects on the sympathetic nervous system” (Calvi et al., 2021).
References
Anna Calvi, Ilaria Fischetti, Ignazio Verzicco, Martino Belvederi Murri, Stamatula Zanetidou, Riccardo Volpi, Pietro Coghi, Stefano Tedeschi, Mario Amore, & Aderville Cabassi. (2021). Antidepressant Drugs Effects on Blood Pressure. Frontiers in Cardiovascular Medicine, 8. -org.ezp.waldenulibrary.org/10.3389/fcvm.2021.704281
Martínez, A., Ibarra, I. A., & Vargas, R. (2019). A quantum chemical approach representing a new perspective concerning agonist and antagonist drugs in the context of schizophrenia and Parkinson’s disease. PLoS ONE, 14(12), 1–12. org.ezp.waldenulibrary.org/10.1371/journal.pone.0224691
Roberta Mazzone, Clemens Zwergel, Marco Artico, Samanta Taurone, Massimo Ralli, Antonio Greco, & Antonello Mai. (2019). The emerging role of epigenetics in human autoimmune disorders. Clinical Epigenetics, 11(1), 1–15.
Weis, W. I., & Kobilka, B. K. (2018). The Molecular Basis of G Protein-Coupled Receptor Activation. Annual review of biochemistry, 87, 897–919.
Yeng-Tseng Wang, & Yang-Hsiang Chan. (2017). Understanding the molecular basis of agonist/antagonist mechanism of human mu opioid receptor through gaussian accelerated molecular dynamics method. Scientific Reports, 7(1), 1–11. org.ezp.waldenulibrary.org/10.1038/s41598-017-08224-2
NURS_6630_Week2_Discussion_Rubric
Excellent
Point range: 90–100
Good
Point range: 80–89
Fair
Point range: 70–79
Poor
Point range: 0–69
Main Posting:
Response to the Discussion question is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources.
40 (40%) – 44 (44%)
Thoroughly responds to the Discussion question(s).
Is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources.
No less than 75% of post has exceptional depth and breadth.
Supported by at least three current credible sources.
35 (35%) – 39 (39%)
Responds to most of the Discussion question(s).
Is somewhat reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module.
50% of the post has exceptional depth and breadth.
Supported by at least three credible references.
31 (31%) – 34 (34%)
Responds to some of the Discussion question(s).
One to two criteria are not addressed or are superficially addressed.
Is somewhat lacking reflection and critical analysis and synthesis.
Somewhat represents knowledge gained from the course readings for the module.
Post is cited with fewer than two credible references.
0 (0%) – 30 (30%)
Does not respond to the Discussion question(s).
Lacks depth or superficially addresses criteria.
Lacks reflection and critical analysis and synthesis.
Does not represent knowledge gained from the course readings for the module.
Contains only one or no credible refere