Introduction to Neuroscience
Walden University Introduction to Neuroscience-Step-By-Step Guide
This guide will demonstrate how to complete the Walden University Introduction to Neuroscience assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for Introduction to Neuroscience
Whether one passes or fails an academic assignment such as the Walden University Introduction to Neuroscience depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for Introduction to Neuroscience
The introduction for the Walden University Introduction to Neuroscience is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
How to Write the Body for Introduction to Neuroscience
After the introduction, move into the main part of the Introduction to Neuroscience assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for Introduction to Neuroscience
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for Introduction to Neuroscience
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Psychiatric mental health nurse practitioners play a fundamental role in the management of psychiatric disorders. Undeniably, their knowledge regarding the pathophysiology of multifarious mental disorders need to be top notch. However, in addition to the pathophysiological knowhow, PMNHPs need to understand the various mechanisms of action of relevant medications and the manner in which they influence the central nervous system to stabilize the neurochemicals responsible for the existence of these conditions. Thus, PMNHPs require to have knowledge concerning the impact of psychopharmacological medications from their agnostic-to-antagonist spectrum of action. In addition, knowing about the roles of g-coupled proteins and ion gated channels in the entire process of managing mental health conditions becomes an important tool for these nurses. Further, other factors such as epigenetics also influence the pharmacologic action of drugs. As such, a collation of the above information may be fundamental in the prescription of medications to clients; hence, their analysis becomes important.
Agonist-To-Antagonist Spectrum of Action of Psychopharmacologic Agents
The prescription of psychopharmacological agents occurs based on the mechanisms of action of each molecule. Fundamentally, pharmacological actions of antipsychotics such as agonism and antagonism principally influences neurotransmitters or receptors. According to scholarship on the matter, agonists are referred to as the kinds of drugs or receptor ligands that bind to certain receptors in order to produce the desired therapeutic effect (Lee & Barron, 2017). Specifically, agonists bind to receptors and modulate the activation of the receptors in order to produce the requisite action. The modulation occurs when the agonists alter the conformation of the receptor in order to optimally open the ion channel as well as induce the maximum frequency of the receptors for binding purposes. As a consequence, a maximum downstream signal transduction that has the capacity to be mediated by a receptor occurs.
The above spectrum then moves to antagonists, which are utilized to stabilize the receptor to the resting phase. In other words, the antagonists are used to return ta receptor to its state when the agonists were not available. However, the resting state occasioned by the antagonists still has certain levels of ion flowing through the channel since the ion channel is not fully closed. Therefore, the agonist-to-antagonist spectrum of pharmacological agents entails agonists that open a receptor channel to maximal frequency and amount via antagonists that retain the resting state of a receptor, and lastly to inverse agonists that close and inactivate the receptor ion channel (Stahl, 2013). In between the antagonists and agonists are partial agonists that partially influences the receptor ion channels in comparison to the two. Further, antagonists have the potential to block everything within the agonist spectrum thus ensuring that the ion channel returns to its resting state. Thus, psychopharmacological agents assume this spectrum when addressing certain mental health conditions.
Comparison of the Actions of G Couple Proteins and Ion Gated Channels
Ion channels are important as regards the selective movement of particular ions across the membrane. One of the types of ion channels include the G couple proteins and ion gated channels. According to studies, both channels are proteins in nature and are embedded within cell membranes and they allow for the passage of ions. G Couple Proteins are composed of a continuous chain having 7 lipophilic helical segments inside the membrane, which allows it to become activated by numerous chemical messengers (Stahl, 2013). Further, the G Protein Couple Receptors are affected by two signal transduction pathways entailing Phosphatidylinositol signal pathway and cAMP signal pathway (Li, Wong, & Liu, 2014). On the other hand, whereas ion channels similarly comprise lipophilic helices in their structures, they attach to different chains hence numerous variants exist. Also called ligand gated channels, ion gated channels experience conformation alteration when a ligand is attached to them leading to the opening of a channel along the membrane to permit the passage of a specific molecule. Thus, unlike the g coupled proteins, the ion gated channels only activates certain ion neurotransmitters to allow for the conductance of specific ions.
Role of Epigenetics in Pharmacologic Action
The pharmacology of epigenetics has assumed significance when it comes to the management of brain disorders. The concept refers to the alterations that result in heritable changes regarding the expression of the gene independent of alterations in the genetic sequence. Studies have demonstrated that epigenetics modulates methylation, ubiquitylation, phosphorylation, as well as acetylation of the deoxyribonucleic acid (DNA) (Valor, 2015). As a consequence, the manner in which the body reacts to standard therapeutic interventions via pharmacological agents is affected. Other studies have revealed that epigenetics changes the remodeling of the chromatin affecting both the response of a patient’s body to a prescription drug as well as diagnostic testing for various conditions.
How This Information Impact the Way Medications are Prescribed
The information above plays a crucial role in the manner in which PMNHP selects medicines for psychiatric patients. During such an exercise, the genetic makeup of a patient as it relates to their ethnicity as well as drug interactions become important. The decision to choose a certain drug will be influenced by the response of a patient as some of them may develop allergies alongside adverse reactions to a drug. For instance, while prescribing lithium 1200mg/day for a patient with type 1bipolar disorder, one must be aware of associated side effects that might impede compliance during care management. Hamlat, O’Garro-Moore, Alloy, and Nusslock (2016) posit that in as much lithium carbonate medication stabilizes manic episodes for patients with bipolar disorder, it can also aggravate vomiting, bilateral hand tremors, and ataxia which can comprise self-medication.
References
Hamlat, E. J., O’Garro-Moore, J. K., Alloy, L. B., & Nusslock, R. (2016). Assessment and Treatment of Bipolar Spectrum Disorders in Emerging Adulthood: Applying the Behavioral Approach System Hypersensitivity Model. Cognitive and behavioral practice, 23(3), 289-299.
Lee, S., & Barron, M. G. (2017). Structure-Based Understanding of Binding Affinity and Mode of Estrogen Receptor α Agonists and Antagonists. PLoS ONE, 12(1), 1–14. https://doi.org/10.1371/journal.pone.0169607
Li, S., Wong, A. H., & Liu, F. (2014). Ligand-gated ion channel interacting proteins and their role in neuroprotection. Frontiers in cellular neuroscience, 8, 125. doi:10.3389/fncel.2014.00125
Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press.
Valor, L. M. (2015). Epigenetic-based therapies in the preclinical and clinical treatment of Huntington’s disease. International Journal of Biochemistry & Cell Biology, 67, 45–48. https://doi.org/10.1016/j.biocel.2015.04.009
The Agonist-to-Antagonist Spectrum of Action of Psychopharmacologic Agents
The agonist-to-antagonist spectrum is made up of two words that are important to be understood singly. An agonist is a chemical that binds to a receptor thereby activating it to trigger a biological response. Antagonist, on the other hand, blocks the response mediated by the agonist. Antagonist causes an action opposite to that of the agonist, which reaction is called reverse agonist, to occur (Stahl, 2013). Once an agonist binds to a receptor, a full/conventional or partial agonist reaction may occur. As the concentration of the agonist increases, the occupancy of receptors also increases, consequently increasing the response (Stahl, 2013). The antagonist effect of a drug occurs when the antagonist increases in concentration thereby surmounting the activation effect of the agonist and inhibiting their response. A full agonist produces the maximal response system while a partial agonist produces a submaximal one.
The Actions of G-Couple Proteins and Ion-Gated Channels
There are two broad families of protein receptors involved in the opening and closing of the postsynaptic ion channels, namely g-couple proteins and ion-gated channels (Laureate Education Producer, 2016i). G protein-coupled receptors/seven transmembrane (7-TM) receptors form the largest protein family (about 600 – 1000 members) and are involved in many normal biological and pathological conditions (Inanobe & Kurachi, 2014). They have a diverse function and recognize many ligands including proteins, small molecules, and photons (Stahl, 2013). They specifically maintain the electrochemical gradient across the cell.
Ligand-gated ion channels (LGICs), on the other hand, are transmembrane ion channels found in the cellular membrane. They help in the opening and closing of the membrane to allow for the passage of ions such as Na+, K+, Ca2+, and/or Cl−. The human genome has over 400 genes for ion channels. Their opening and closing are dependent on the attachment of a chemical messenger, a ligand, such as a neurotransmitter (Inanobe & Kurachi, 2014).
The Role of Epigenetics in Pharmacologic Action
Different patients respond differently to various medications due to the genetic alterations that occur at an individual level. Epigenetic allows the understanding of these modifications in gene expressions that occurs in the DNA sequence of a gene for some patients. These genetic modifications are called epigenetic alterations. They include methylation, phosphorylation, acetylation, and ubiquitylation of DNA (Swathy & Banerjee, 2017). These alterations make many patients not to respond to standard therapies. The alterations not only regulate gene expression but also other cellular and biological functions related to allostasis, homeostasis, and disease (Rasool et al., 2015). These processes generally influence pharmacogenetics activities such as the contribution of receptors, drug transporters, and drug-metabolizing enzymes.
Impacts of Epigenetics in Pharmacologic and Examples of Psychiatric Mental Health Cases
The epigenetic alterations that occur at individual levels require doctors to provide personalized treatments to patients. Since epigenetic alterations differ from one patient to the other, physicians should do genetic screenings of patients to guide disease prediction and prevention and decision making on the medical recommendations and lifestyle and disease management practices that are best at an individual level (Rasool et al., 2015). For instance, in the case of Schizophrenia, the genetic modifications occur in the histones or DNA such as DNA methylation. For histone modification, HDAC (histone deacetylase) inhibitors drugs are recommended because they up-regulate the levels of reelin and GAD67. HMT (histone demethylase) inhibitors also prevent the demethylation of the H3K4 histone protein. As for DNA methylation, DNMT (DNA Methyltransferases) inhibitors are recommended because they raise the reeling levels of proteins and protein and GAD67 (Swathy & Banerjee, 2017). This requires physicians to make an individual genetic screening of a patient to determine the particular epigenetic alteration they experience before recommending drug prescriptions that are best and specific to them.
References
Inanobe, A., & Kurachi, Y. (2014). Membrane channels as integrators of G-protein-mediated signaling. Biochimica Et Biophysica Acta (BBA)-Biomembranes, 1838(2), 521-531.
Laureate Education (Producer). (2016i). Introduction to psychopharmacology [Video file]. Baltimore, MD: Author.
Rasool, M., Malik, A., Naseer, M. I., Manan, A., Ansari, S. A., Begum, I., & Kamal, M. A. (2015). The role of epigenetics in personalized medicine: challenges and opportunities. BMC medical genomics, 8(S1), S5.
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
Swathy, B., & Banerjee, M. (2017). Understanding epigenetics of schizophrenia in the backdrop of its antipsychotic drug therapy. Epigenomics, 9(5), 721-736.