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{"id":3473,"date":"2020-08-18T12:14:19","date_gmt":"2020-08-18T12:14:19","guid":{"rendered":"https:\/\/nursingwritersbureau.com\/?p=3473"},"modified":"2020-08-18T12:14:19","modified_gmt":"2020-08-18T12:14:19","slug":"discussion-foundational-neuroscience","status":"publish","type":"post","link":"https:\/\/nursingwritersbureau.com\/discussion-foundational-neuroscience\/","title":{"rendered":"Discussion: Foundational Neuroscience"},"content":{"rendered":"TO DO A REPLY COMMENT TO POST 1 and 2 WITH TWO APA REFERENCES EACH ABOVE 2013.<\/p>\n
POST 1<\/p>\n
An agonist to antagonist to inverse agonist spectrum<\/p>\n
Psychoactive medications vary in how they affect activity at the synapse.\u00a0 Agonists increase the neurotransmitter effect while antagonists block the neurotransmitter effect (Barron, 2018). There are gradients of how medications act creating a spectrum of influence on receptors.\u00a0 Agonists can occur naturally as neurotransmitters that stimulate receptors.\u00a0 Some medications also act as agonists to stimulate receptors, but medications can stimulate receptors to varying degrees (Stahl, 2013).\u00a0 This creates the spectrum of how medications variably affect neurotransmitters.\u00a0 The medications that stimulate receptors but do so less than full agonists are partial agonists or stabilizers.\u00a0 Antagonists have no activity of their own except to block the activity of the agonists, sometimes antagonists are called silent (Stahl, 2013).\u00a0 At the opposite end of the spectrum from agonists are inverse agonists. These medications block agonists and decrease activity to below the normal baseline level when there is no agonist present (Stahl, 2013).<\/p>\n
G Couple proteins and Ion gated channels<\/p>\n
Ion gated channels are proteins that form pores in cell membranes (Inanobe & Kurachi, 2014).\u00a0 These pores are the channels that allow movement across the cell membrane and are controlled by several mechanisms. The pore may open due to the voltage difference across the membrane (Ianonobe & Kurachi, 2014).\u00a0 Ligand-gated channels have a domain extracellular that associates with small chemicals and regulatory proteins (Ianonobe & Kurachi, 2014).\u00a0 A domain is a protein that has its own stable structure (Genscript, 2018). Ion channels gated by ligands can be opened or closed by a neurotransmitter that is specific to a ligand binding and causing a very short, brief open active state that occurs in milliseconds (Inanobe & Kurachi, 2014).\u00a0 The ligand-gated channels can also be opened when metabotropic receptors that have G protein-coupled receptors are stimulated by G protein signaling (Inanobe & Kurachi, 2014).\u00a0 The G protein-coupled ion gated open response is slower and is longer lived than the neurotransmitter ion channel opening (Ianonobe & Kurachi, 2014).\u00a0 In summary, an ion gated channel is a throughway to the cell and this throughway is stimulated to be opened or closed by various mechanisms.\u00a0 One of the ways the ion gated channel is stimulated to open is through G couple proteins.<\/p>\n
Epigenetics in pharmacologic action<\/p>\n
Genes are inherited from each parent.\u00a0 But epigenetics looks at if the gene is developed into its specific RNA and protein or if the gene is silenced and ignored (Stahl, 2013).\u00a0 Childhood stress has been found to deactivate the receptors for glucocorticoids (Rosenfield & Ziff, 2018).\u00a0 Because the receptors are deactivated people grow up with disrupted feedback.\u00a0 The glucocorticoids continue to be made by the body in greater amounts because they are not detected normally.\u00a0 DNA methylation occurs and creates a barrier to normal genetic codes (Rosenfield & Ziff, 2018).\u00a0 Long-term effects from childhood stressors are chronic inflammation, diabetes, heart disease, obesity, schizophrenia and major depressive disorder (Rosenfield & Ziff, 2018).\u00a0 Cells including neurons respond to life stressors by reacting to genetics.\u00a0 Genes may be silenced or activated but the expression of genetics can vary depending on stress (Stahl, 2013).<\/p>\n
Possible Impact on Clients<\/p>\n
Psychopharmacology is important because of the impact interactions can have on patients.\u00a0 As future prescribers, it is important to be aware of patient differences and how illness affect patient\u2019s ability to metabolize medications (Laureate Education, 2012).\u00a0 It is also important to be aware of drug interactions with other medications, foods, and metabolism.\u00a0 For example, Wellbutrin is primarily metabolized by CYP2B6.\u00a0 So, Wellbutrin can react with other medications that are inhibitors or inducers of CYP2B6 (Drugs.com, 2018).\u00a0 Plavix and Ticlid are CYP2B6 inhibitors and can increase bupropion levels (Drugs.com, 2018).\u00a0 People also metabolize medications differently.\u00a0 There are four classes of metabolizers from ultra-extensive metabolizers to poor metabolizers (Barron, 2018).\u00a0 Knowing the type of metabolizer that the patient is can be helpful in tailoring their medication and dosage.\u00a0 Epigenetics teaches us that people with trauma can have their gene expression altered by DNA methylation.\u00a0 Trauma can lead to metabolic type diseases as well as depression and schizophrenia.\u00a0 As a client example, a 17-year-old male was admitted for being increasingly physically and verbally abusive to his entire foster family.\u00a0 The client had pushed down a foster brother and punched and kicked his foster mom and dad.\u00a0 This client had been taken away from his biological mom around age 5 due to her drug use, neglect then jail.\u00a0 He was then placed with his maternal grandmother who could not handle his behavior.\u00a0 The client then was placed in numerous foster homes for brief periods of time.\u00a0 He acted appropriately in the Psychiatric care center, so he could control his behavior when multiple security\/ authority figures were present.\u00a0 The client had been on Wellbutrin at home and when he had symptoms of insomnia and aggression his Wellbutrin was increased.\u00a0 He was taken off Wellbutrin and started on another medication.\u00a0 Some of the more common side effects of Wellbutrin are sleep disturbance (45%), agitation (32%), irritability, and anxiety (Drugs.com, 2018).\u00a0 This patient\u2019s history of trauma and aggression set him up for depression, anxiety and irritability then when he had increased symptoms with the medication it was increased to the maximum dose as an outpatient.\u00a0 He became increasingly agitated and then violent which led to his admission to an inpatient psychiatric facility.<\/p>\n
References<\/p>\n
Barron, S. (2018). Psychopharmacology. Nobia textbook series:\u00a0 Psychology<\/em>. https:\/\/doi.org\/nobaproject<\/p>\nDrugs.com. (2018). Wellbutrin. Retrieved from https:\/\/www.drugs.com\/pro\/wellbutrin.html<\/p>\n
Genscript. (2018). Domain. Retrieved from https:\/\/www.genscript.com\/molecular-biology-glossary\/819\/domain<\/p>\n
Inanobe, A., & Kurachi, Y. (2014, February). Membrane channels as integrators of G-protein mediated signaling. Biochimica et Biophysica Acta (BBA) Biomembranes<\/em>, 1838<\/em>(2), 521-531. https:\/\/doi.org\/10.1016\/j.bbamem.2013.08.018<\/p>\nLaureate Education. (2012). Introduction to advanced pharmacology<\/em>[Video file]. Retrieved from Walden University<\/p>\nRosenfield, I., & Ziff, E. (2018). Epigenetics:\u00a0 The evolution revolution. Retrieved from https:\/\/www.nybooks.com\/articles\/2018\/06\/07\/epigenetics-the-evolution-revolution\/<\/p>\n
Stahl, S. M. (2013). Stahl\u2019s essential psychopharmacology:\u00a0 Neuroscientific basis and practical applications<\/em> (4th ed.). Retrieved from https:\/\/stahlonline-cambridge-org.ezp.waldenulibrary.org<\/p>\nPOST 2<\/p>\n
Agonist\u00a0to Antagonist Spectrum<\/strong><\/p>\nMost drugs act as either\u00a0agonists\u00a0or antagonists at receptors in response to chemical messages in the brain.\u00a0 An\u00a0agonist, which can be described as partial or inverse, binds to the receptor to produce an effect.\u00a0 Antagonists also bind to receptors but does not produce a response, rather blocks that receptor to a natural\u00a0agonist\u00a0(Pleuvry, 20004).\u00a0 It is important to acknowledge that\u00a0agonists\u00a0and inverse\u00a0agonists\u00a0can be reversed by competitive antagonists.\u00a0 In reference to atypical psychotropic drugs (APD), the blockade of\u00a0serotonin\u00a0receptors (5-HT2A) along with the weak antagonism of dopamine receptor (D2) is critical in potency and efficacy, as typical APD have tendency to antagonize D2 receptors more potently than 5-HT2A receptors (Kusumi,\u00a0Boku, &\u00a0Takahashi, 2014).<\/p>\n
G-coupled Protein and Ion-gated Channels<\/strong><\/p>\nG-protein linked receptors are important to clinicians with to target specific receptors with psychotropic drugs (Stahl, 2013).\u00a0 Nonetheless, all\u00a0agonists\u00a0do not produce an active state of G-protein-coupled-receptors as in constitutive activity of receptors for\u00a0benzodiazepines,\u00a0serotonin, and other G-protein linked receptors.\u00a0 Contrarily, ion channels function as a result of neurotransmitter ligands at receptors.\u00a0 Numerous drugs act at ion-channel complexes altering flow of ions through the channels due to the transduction of the signal at receptors (Stahl, 2013).\u00a0 As a result of the changes of flow of ions, drugs that act on\u00a0ionotropic\u00a0receptors tend to act immediately while G-protein linked receptors act at lower frequencies.<\/p>\n
Epigenetics\u00a0in\u00a0Pharmacologic\u00a0Action<\/strong><\/p>\nThe lack of response to standard therapies in certain individuals because of various molecular alterations can be due to genetic\u00a0heterogenecity\u00a0and epigenetic alterations (Rasool\u00a0et\u00a0al., 2015).\u00a0 Epigenetic modifications can occur as a result of various chemical compounds in the biological system, changing gene expression.\u00a0 Environmentally and biologically influenced alterations can lead to disorders, therefore clients with epigenetic alterations may require drugs used for personalized medicine based on their personal\u00a0genomic\u00a0profile.<\/p>\n
Impact on How Medicine is Prescribed<\/strong><\/p>\nUnderstanding the\u00a0agonistic\/antagonistic effects of medications along with the prescribing of medications specific to G-protein coupled receptors, and personalized medication profiles required by epigenetic alterations found in certain cases is important to\u00a0PMHNP’s\u00a0who may prescribe psychotropic medications to these clients.\u00a0 Studies have found an existence of constitutive receptor activity in\u00a0benzodiazepine\u00a0receptors and G-protein\u00a0coupled receptors and may be present in mutated strains exhibiting\u00a0underactive\u00a0behavior that can lead to inherited diseases such as congenital hypothyroidism and diabetes\u00a0insipidus\u00a0(Rasool\u00a0et\u00a0al., 2015).\u00a0 For schizophrenic clients at greater risk for developing\u00a0extrapyramidal\u00a0symptoms (EPS), it is known that\u00a0risperidone\u00a0equally occupies D2 and 5-HT2A receptors increasing the frequency of EPS, while\u00a0clozapine\u00a0more potently occupies 5-HT2A receptors than D2 receptors, rarely producing EPS (Kusumi,\u00a0Boku, &\u00a0Takahashi, 2014).\u00a0 It is the responsibility of the PMHNP to understand their clients’ profiles and medical histories in order to properly prescribe the most effective medications with the least adverse effects.<\/p>\n
REFERENCES<\/p>\n
Kusumi, I., Boku, S., & Takahashi, Y. (2014).\u00a0 Psychopharmacology of atypical antipsychotic drugs: From the recpetor binding profile to neuroprotection and neurogenesis.\u00a0\u00a0Psychiatry and Clinical Neurosciences, 69<\/em>(5): 243-258. doi: 10.1111\/pcn.12242.<\/p>\nPleuvry, B. (2004).\u00a0 Receptors, agonists, and antagonists.\u00a0\u00a0Anaesthesia & Intensive Care Medicine, 5<\/em>(10): 350-352.\u00a0 doi: 10.1383\/anes.5.10.350.52312.<\/p>\nRasool, M., Malik, A., Naseer, M., Manan, A., Ansari, S., Begum, I.,…Gan, S. (2015).\u00a0 The role of epigenetics in personalized medicine: Challenges and opportunites.\u00a0\u00a0BMC Medical Genomics, 8<\/em>(Suppl 1): S5.\u00a0 doi: 10.1186\/1755-8794-8-S1-S5.<\/p>\nStahl, S. (2013).\u00a0\u00a0Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications<\/em>\u00a0(4th ed.).\u00a0 New York, NY: Cambridge University Press.<\/p>\n \n
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