Want create site? With Free visual composer you can do it easy.

Discussion NURS-6630N-37  Psychopharmacology and the role of Agonists &amp Antagonists

Discussion: NURS-6630N-37  Psychopharmacology and the role of Agonists & Antagonists

Week 2 Discussion Main Post

Psychopharmacology and the role of Agonists & Antagonists
To understand the role of an agonist and an antagonist, we must first know what
they do.  An Agonist is a chemical (i.e., A drug) that activates a receptor to produce a
biological response (Berg & Clarke, 2018).  There are many agonists; however, we will
focus on only four for this discussion.  The first is the endogenous agonist, which the
body naturally produces, the second is the full agonist, which will produce the maximal
response the system is capable of, third is the partial agonist, while at maximum
occupancy, it will not create a maximal response and will act as an antagonist in the
presence of a full agonist, and the fourth, the inverse agonist will bind to a receptor and
produce the opposite effect of an agonist (Berg & Clarke, 2018).
Antagonists are chemicals that block the action of other substances.  There are three
types of antagonists: competitive antagonists, which compete for the same binding site
as an agonist and can be reversible or irreversible.  Second, a non-competitive
antagonist is insurmountable to any maximum response by an agonist by being
irreversible or binding to an allosteric site.  The third is the uncompetitive antagonist,
which needs an agonist activation before binding to an allosteric site (Arunlaskshana,
Schlild & Jenkinson, 1997).

Ion Gated Channels and G Coupled Proteins
Ion gated channels and G coupled proteins are transmembranes with ligand binding
sites, and both change their shape in response to a ligand (Stern, Fava, Wilens &
Rosenbaum, 2016).  The similarity ends there; ion gated channels work by an
electrochemical gradient allowing ions to flow back and forth across the membrane to
produce an action potential, whereas the G coupled protein activation will lead to
activation of various second messengers systems, modulating the activity of
downstream effectors and intercellular responses (Vaidehi et al., 2002).

Epigenetics Contribution to Pharmacologic Action
Epigenetics is the study of how our genes get expressed based on our behavior and
environment, and DNA itself remains unaltered (Stern, Fava, Wilens & Rosenbaum,
2016).  Gene expression varies and changes over time with our behaviors and the
environment in which we live (Stefanska & MacEwan, 2015).  Drug treatments or cures

may lie in understanding the mechanisms of how epigenomes work and their effects on
disease.
As a psychiatric mental health nurse practitioner (PMHNP), my patient’s safety is
paramount.  I must understand how the mechanisms of action of the medication(s) I
prescribe work, what side effects or adverse reactions they might cause, and the dose
amount of the drug to elicit the desired result.  For instance, when prescribing lithium to
a patient with bipolar disorder, the PMHNP must know that lithium will decrease
dopamine and glutamate and increase GABA.  Lithium also has a small therapeutic
window, and the patient must have their blood tested regularly.  If the level is too low,
lithium will have no medicinal value, and if the level is too high, it could harm or kill the
patient.  My role is to provide excellent patient care to bring about better patient
outcomes.

References
Berg, K. A. & Clarke, W. P. (2018). Making Sense of Pharmacology: Inverse Agonism
and Functional
Selectivity. International Journal of Neuropsychophamacology, 21(10): 962-977.
Arunlakshana, O., Schild, H. O., & Jenkinson, D. H. (1997). Some quantitative uses of
drug antagonists.
British Journal of Pharmacology, 120(Suppl 1): 148-150.
Stern, T. A., Fava, M, Wilens, T. E., & Rosenbaum, J. F. (2016). Massachusetts
General Hospital
Psychopharmacology and Neurotherapeutics (1 st  ed.). St. Louis, MO. Elsevier.
Vaidehi, N., Floriano, W.B., Trabanino, R…..Goodard, W.A. (2002).  Prediction of
structure and function
of G protein-coupled receptors. Proceedings of the National Academy of Sciences,
99(20): 12622-
12627.
Stefanska, B. & MacEwan, D. J. (2015). Epigenetics and pharmacology. British Journal
of Pharmacology
172(11): 2701-2704.

BUCHANAN INITIAL

COLLAPSE

Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents,
including how partial and inverse agonist functionality may impact the efficacy of
psychopharmacologic treatments.

Drugs with affinity and intrinsic efficacy are noted as agonists.  Affinity can be defined as
binding target receptors. Intrinsic efficacy is those that change the receptor to produce an action
or a response. In reviewing antagonists, they have affinity but have no action or intrinsic efficacy
(response). So, the antagonists will bind to the target receptor producing an action response. If
we were to have an “inverse” agonist which is known as a ligand, and it binds to the same
receptor site as an agonist we would create the opposite effect by suppressing the receptor signal.
An example would be the opposite effect of a sedative: agonism leads to the wanted effects of
the pharmacological agent, (sleep) and the ligand causing the opposite effect (wake/insomnia).
Notable is while the agonist increases the level of the activity of the agent the opposite, we know
is true from the “inverse” agonist, decreasing the activity below the basal level. A full agonist
has a 100% efficacy, and 0% efficacy is noted in a neutral “antagonist” and the inverse is evident
for a value of negative or <0% (Berg, & Clarke, 2018; Khilnani & Khilnani, 2011).

Compare and contrast the actions of g couple proteins and ion gated channels.

To compare the actions of a G-protein (largest and most versatile) couple receptor (GPCR)
“open” ion channels. It is a highly diverse protein which recognizes a wide range of ligands,
small mol. and proteins which allow ions to go in and out of a cell. Remember they open ion
channels (specialized proteins) allowing passageway where these charged channels can cross
through plasma membrane and down to the electrochemical gradient (Berg, & Clarke, 2018).

Ion channel (linked receptors) bind a ligand, open a channel where the membranes allow for
specific ions to pass through. GPCR “protein” bind a ligan and activate a G-protein membrane
which can react to an ion or an enzyme in the membrane. These are proteins that convert
extracellular signaling to intracellular responses (Berg, & Clarke, 2018; Khilnani & Khilnani,
2011).
.
Explain how the role of epigenetics may contribute to pharmacologic action
To define epigenetics, we must understand that its role is look at how specific behaviors and
environment cause changes and affect our genes. These are not considered “genetic” in your
DNA sequence changing; however, epigenetic changes are reversible and do change how the
body reads the sequence (DNA). How this contributes to pharmacological action is through
epigenetic therapy, influencing the reading of the sequencing DNA and by influencing the
pathways of disease directly, i.e. diabetes, Alzheimer’s, cancer and mental illness (Stefanska,&
MacEwan, 2015).

Explain how this information may impact the way you prescribe medications to patients.
Include a specific example of a situation or case with a patient in which the psychiatric
mental health nurse practitioner must be aware of the medication’s action

Through epigenetic effect one can view the independent effect or therapeutic potential.
Development approaches and implementation of pharmacological substances are actuated by the
drug selectivity and ad the intrinsic efficacy. Understanding that antidotes or almost all receptors
have a fundamental activity, and antagonist drugs have an inverse property. The psychiatric
mental health nurse practitioner needs to be aware of the whole person, both psychological and
physiological aspects. Someone with heart failure might not have the benefits of specific
psychiatric medications due to the action potential or the pathway/response. Some of the
medications we consider will enhance one’s chronic disease (exacerbate it), such as diabetes or
kidney disease. All of these factors combined with the behavioral aspect need to be considered,
even those that have a high abuse potential (Angell & Bolden, 2015). Additionally, as with all
medications a drug-drug interaction should always be on the forefront of use.

Angell, B., & Bolden, G. B. (2015). Justifying dication decisions in mental health care:
Psychiatrists' accounts for treatment recommendations. Social science & medicine (1982), 138,
44–56. https://doi.org/10.1016/j.socscimed.2015.04.029

Berg, K. A., & Clarke, W. P. (2018). Making Sense of Pharmacology: Inverse Agonism and
Functional Selectivity. The international journal of neuropsychopharmacology, 21(10),
962–977. https://doi.org/10.1093/ijnp/pyy071
Khilnani, G., & Khilnani, A. K. (2011). Inverse agonism and its therapeutic significance. Indian
journal of pharmacology, 43(5), 492–501. https://doi.org/10.4103/0253-7613.84947
Stefanska, B., & MacEwan, D. J. (2015). Epigenetics and pharmacology. British journal of
pharmacology, 172(11), 2701–2704. https://doi.org/10.1111/bph.13136
Discussion Main Post Wk 2- Bailey Zaruba
COLLAPSE

Explain the agonist-to-antagonist spectrum of action of
psychopharmacologic agents, including how partial and inverse agonist
functionality may impact the efficacy of psychopharmacologic treatments.

Discussion NURS-6630N-37  Psychopharmacology and the role of Agonists &amp Antagonists

Discussion NURS-6630N-37  Psychopharmacology and the role of Agonists &amp Antagonists

Click here to ORDER an A++ paper from our MASTERS and DOCTORATE WRITERS:Discussion: NURS-6630N-37  Psychopharmacology and the role of Agonists & Antagonists

The agonist-to-antagonist spectrum is made up of agonists, partial
agonists, and antagonists.  Agonists are drugs that bind to receptors stimulating
the intended reaction. These are transmitters that are naturally occurring and
facilitate the stimulation of receptors. Drugs dual as neurotransmitters allowing
receptors to be stimulated creating an intended response. Partial agonists have
the goal of activating receptors but lack the ability to create a full response from
said receptors. Antagonists are drugs that bind to receptors and block or slow the
intended reaction. Antagonists have the capability to block the inverse agonists
and anything along the agonist spectrum (Nguyen, 2018).
When a dose of partial agonists increases, a plateau in analgesic activity will
occur preventing additional relief as the dose increases. This also can increase
the occurrence of adverse effects. Examples of these types of medications or
partial agonists include buprenorphine and tramadol. Inverse agonists can
decrease receptor activity allowing for strong and weak inverse agonists via
ligands (Fudin, 2018). With this knowledge, there is greater control over select
receptor function resulting in improved treatment. It is crucial to consider where a
medication falls on the spectrum to adequately treat patients.
Compare and contrast the actions of g couple proteins and ion gated
channels.
G couple proteins are integral membrane proteins utilized by cells to
convert extracellular signals to intracellular responses. The responses included
are hormones, neurotransmitters, and different senses, such as vision, smell,
and taste. There are two receptor proteins of which function as a gate to open
and close postsynaptic ion channels. One of these receptors, the ionotropic
receptor, has direct links to ion gated channels. Ion gated channels encompass a
membrane of proteins of excitable cells that allows ions to pass under specific
circumstances. These ion-gated channels can be ligand-gated or voltage-gated.
The primary functionality of g couple proteins and ion gated channels include the
extracellular domain and the membrane-spanning domain. A specific family of

neurotransmitters, metabotropic receptors, activates G-proteins (G-protein-
coupled receptors) which affect ion gated channels to ensure activation and
interaction occurs at the specific site- an ion channel or enzyme (Zhao et al.,
2016).
Explain how the role of epigenetics may contribute to pharmacologic
action.
Epigenetics is the concept that the function of a gene may be altered
without changing the code. This leads researchers to believe that it is heritable,
as the structure of the DNA molecule is altered.  Epigenetics plays a role in the
action of medications specifically those that affect the chromatic structure and
older medications. Epigenetics plays a crucial role in the development of certain
diseases and neurological disorders. Specific epigenetic regulatory mechanisms
are associated with these neurological disorders such as depression. These
mechanisms include non-coding RNA regulation, DNA methylation, and histone
modification. This modification includes things like phosphorylation and
methylation, thus activating gene transcriptions. Due to this, these epigenetic
modifications have allowed researchers to understand different
disorders (Camprodon & Roffman, 2016).
Explain how this information may impact the way you prescribe
medications to patients. Include a specific example of a situation or case
with a patient in which the psychiatric mental health nurse practitioner
must be aware of the medication’s action.
It’s crucial to understand the biological mechanisms that allow the brain to
function and dysfunction so further research can be completed regarding the
development of new psychological remedies. There remain gaps in knowledge
between this information and clinical judgment. As a nurse practitioner, it is key
to know the biological components including the mechanisms of
neurodevelopment, neurotransmission, neurodegeneration, and cellular and
molecular substrates to further incorporate the information in our practice and
educate our patients.  A good example of this is when prescribing
benzodiazepines. Typically, benzos are prescribed to help manage and treat
anxiety. Unfortunately, the longer the treatment with benzodiazepines, the
increased tolerance resulting in the patient requiring higher and higher doses of
the medication. As doses increase, so do side effects. Then when the medication

is discontinued, the patient may experience symptoms of withdrawal. This is
exactly why benzodiazepines should not be prescribed to vulnerable populations
due to misuse and increased risk of withdrawal (Camprodon & Roffman, 2016).

References

Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric neuroscience: Incorporating
pathophysiology into clinical case formulation. In T. A. Stern, M. Favo, T. E.
Wilens, & J. F. Rosenbaum. (Eds.)., Massachusetts General Hospital
psychopharmacology and neurotherapeutics. Elsevier.

 

Fudin, J. (2018, January 6). Opioid agonists, partial agonists, antagonists: Oh
My! https://www.pharmacytimes.com/view/opioid-agonists-partial-agonists-
antagonists-oh-my
Nguyen, A. (2018). Agonists and
Antagonists. https://lx.uts.edu.au/pharmacology/article/agonists-and-antagonists/
Zhao, J., Deng, Y., Jiang, Z., & Qing, H. (2016, March 24). G protein-couple receptors
(GPCRs) in Alzheimer’s Disease: A focus on BACE1 related GPCRs. Frontiers in
Aging Neuroscience, 8. https://doi.org/10.3389/fnagi.2016.00058
Week 2 Post

COLLAPSE

1. Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents, including
how partial and inverse agonist functionality may impact the efficacy of psychopharmacologic
treatments.
Agonists are drugs that activate specific receptors in the brain. Complete agonist opioids
fully activate opioid receptors in the brain, resulting in a complete opioid effect.
Examples of complete agonists are heroin, oxycodone, methadone, hydrocodone,
morphine, and opium. Partial agonist opioids activate opioid receptors in the brain, but to
a much lesser extent than full agonists. Buprenorphine is an example of a partial agonist.
Antagonists are drugs that block opioids by binding to opioid receptors without activating
them. Antagonists do not cause opioid effects and block complete agonist opioids.
Examples are naltrexone and naloxone (Ihs.gov)
1. Compare and contrast the actions of g couple proteins and ion gated channels.

Ligand-gated ion channels are transmembrane protein complexes that guide the flow of
ions through the pores of the channel in response to neurotransmitter binding. Ligand-gated ion
channels are different from voltage-gated ion channels that are sensitive to membrane potentials
and GPCRs that use a second messenger. In general, neurotransmitter receptors trigger fast or
slow effector systems. Fast-acting neurotransmitter receptors are either ion channels themselves
(eg, NMDA glutamate receptors) or are bound to ion channels. The flow of ions through the
channels activated by these transmitters causes rapid changes in membrane potential and neural
activity. Other neurotransmitter receptors, including a large family of g protein-coupled receptors
(GPCRs), act through a slower second messenger system. Such second messenger systems
usually involve a continuous multi-enzyme cascade (Stern et al., 2016).
1. Explain how the role of epigenetics may contribute to pharmacologic action.

The term epigenetics refers to the genetic information "above" or "above" the information
encoded only by our genetic code. Epigenetic regulation of gene activity has been shown
to be important for maintaining the normal phenotypic activity of cells and plays a role in
diseases such as cancer and neurodegenerative diseases such as Alzheimer's disease.
However, epigenetics can cause illness in people with untouched, unmutated DNA. A
new class of drugs regulates epigenetic mechanisms to combat human pathology. This
issue of the report describes an understanding of epigenetics associated with human
disease and advances in the ability to control these mechanisms through pharmacological
means. Pain management is a good example of how pharmacology has evolved over
time-from drugs with unknown ingredients that helped to chemically synthesized purified
compounds with known structures and activities. Pharmacology has our understanding
and has developed the development of therapeutically useful compounds (Stefanska &
MacEwan, 2016)
1. Explain how this information may impact the way you prescribe medications to patients. Include
a specific example of a situation or case with a patient in which the psychiatric mental health
nurse practitioner must be aware of the medication’s action.
This information influences how the drug is prescribed to the patient by assessing each
patient individually and how the drug affects the patient in the long run. For example,
multiple patients with a similar diagnosis of the neurodegenerative disorder may be
affected by many factors such as genetic testing, a history of others, and general health

due to possible effects during treatment. Based on it, it may be treated differently.  Due to
pharmacodynamics, kinetics, and metabolic rate, some medicines work in one patient and
not in others. In contrast, other patients may require multiple trials and detailed
examination of effective medications before starting treatment. Factors such as the
patient's age, race, and gender can help healthcare providers decide how to treat their
condition.

References

Ihs.gov. (n.d.). Pharmacological Treatment | Medication Assisted Recovery. Opioids. Retrieved March 9,
2022, from https://www.ihs.gov/opioids/recovery/pharmatreatment/
Stefanska, B., & MacEwan, D. J. (2016). Epigenetics and pharmacology. British Journal of
Pharmacology, 172(11), 2701–2704. https://doi.org/10.1111/bph.13136
Stern, T. A., Fava, M., Wilens, T. E., Rosenbaum, J. F., & Massachusetts General Hospital.
(2016). Massachusetts General Hospital comprehensive clinical psychiatry. Elsevier.

Agonist-to-antagonist spectrum of action of psychopharmacologic; agents partial and inverse
agonist functionality of psychopharmacologic treatments.

Ligands could act either as agonists with various degrees of intrinsic efficacy, or as
antagonists with zero intrinsic efficacy (Costa and Herz, 1989). The example of this is the drug
called Memantine used in the treatment of Alzheimer's disease. Memantine is a NMDA
antagonist with zero intrinsic efficacy; This drug blocked or dampened the excitotoxic injury
caused by agonist. Inverse agonists can also have different degrees of negative intrinsic efficacy,
which can result in strong and weak (partial) inverse agonists (Costa and Herz, 1989) In their
experiments with wild-type, endogenously expressed delta opioid receptors in membranes of
NG108-15 neuroblastoma cells, found that many ligands previously characterized as antagonists
decreased constitutive receptor-stimulated GTPase activity. Since their effect was opposite to
that of agonists, such ligands were named “inverse” agonists (Costa and Herz, 1989). These
activation influences pharmacological activity to work in an opposite way.

Compare and contrast the actions of g couple proteins and ion gated channels
The actions of g protein coupled receptors (GPCRs) are to integrate membrane proteins
used by cells to convert extracellular signals into intracellular responses (Rosenbaum, et al.,
2009). This includes neurotransmitter response, hormones responses, olfaction, vision, and taste
signals responses. The most important characteristic of G couple proteins is the seven
transmembrane receptors. The wide range of ligands bind to GPCR and the GPCR undergo
conformational changes creating a second messenger which usually involve sequential multi-

enzyme cascades that interacts with either an ion channel or an enzyme in the membrane
(Rosenbaum, et al., 2009). On the other hand, Ion channels are integral membrane proteins that
form a pore to allow the passage of specific ions by passive diffusion. Ion gated channels work
rapidly in altering the membrane potential and neuronal activity (Stern, et. al., 2016). These
channels undergo conformational changes from closed to open states, and once open, channels
allow the passage of thousands of ions (Stern, et. al., 2016). Both the g couple proteins and the
ion gated channel react to Ligands.

Explain how the role of epigenetics may contribute to pharmacologic action.

The role of epigenetic and their contribution to pharmacologic action can be well
explained on this chronic mental illness of schizophrenia. For instance, Epigenetic revealed
decreased levels in reelin and GAD67, the demethylation of H3K4 histone protein, and
Tranylcypromine, an antidepressant HMT inhibitory property in schizophrenia. The example of
Pharmacologic action: Histone Deacetylase inhibitor is a class of drug that can inhibit both reelin
and GAD67; And DNA demethylate inducers (medications such as Clozapine and Sulpiride)
have been shown to induce demethylation which would pharmacologically induce the removal of
methyl groups (Gavin & Sharma, May 2010). This study showed that although it may not be
possible to fully reverse schizophrenia. However, these recent findings suggest that it is possible
to treat patients with schizophrenia, alleviate symptoms, or improve the efficacy of antipsychotic
medication (Gavin & Sharma, May 2010).

Epigenetic impact on prescribing medications to patients; example of a situation or case

The advancement in epigenetic and Pharmacology will impact the way PMHNP
prescribed treatment for their patients. Many diseases, including mental illnesses, heart disease,
cancer and diabetes are influenced by epigenetic mechanisms. Understanding epigenetic of any
chronic conditions, and the ability to influence their pathways directly by the use of
pharmacological agents may be the best approach PMHNP have when it comes to managing
their patients. For instance, when treating a schizophrenia, the PMHNP must use treatment that is
able to target histones modifications and DNA methylation to inhibit reelin, GAD67, and DNA
demethylate to alleviate symptoms, or improve the efficacy of antipsychotic medication (Gavin
& Sharma, May 2010).

References

Costa T., Herz A. (1989). Antagonists with negative intrinsic activity at delta opioid receptors
coupled to GTP-binding proteins. Proc Natl Acad Sci USA 86:7321–7325. [PMC free article]
[PubMed] [Google Scholar]

Gavin D., P, Sharma R., P. (May 2010). "Histone modifications, DNA methylation, and
schizophrenia". Neuroscience and Biobehavioral Reviews. 34 (6): 882–8.
doi:10.1016/j.neubiorev.2009.10.010. PMC 2848916. PMID 19879893.

Rosenbaum, D. M., Rasmussen, S. G., and Kobilka, B. K. (2009). The structure and function of
G-protein-coupled receptors. Nature 459, 356–363. doi: 10.1038/nature08144

Roth TL, Lubin FD, Sodhi M, Kleinman J., E. (September 2009). "Epigenetic mechanisms in
schizophrenia". Biochimica et Biophysica Acta (BBA) – General Subjects. 1790 (9): 869–77.
doi:10.1016/j.bbagen.2009.06.009. PMC 2779706. PMID 19559755.

Stern, T. A., Fava, M., Wilens, T. E., & Rosenbaum, J. F. (2016). Massachusetts General Hospital
psychopharmacology and neurotherapeutics (pp. 1–19). Elsevier.

week 2 Discussion

COLLAPSE

Explain the agonist-to-antagonist spectrum of action of psychopharmacologic
agents, including how partial and inverse agonist functionality may impact the
efficacy of psychopharmacologic treatments
An agonist drug combines with a receptor to mimic or enhance the effects of a neurotransmitter while an
antagonist drug blocks or reduces the effect of a transmitter. A partial agonist can bind to the receptor but
is unable to exert the full force enhancement effect of the neurotransmitter and an inverse agonist might
be able to bind to the receptor but has an opposite effect on the target transmitter. A partial agonist may
require a higher dose than a normal agonist to have a therapeutic effect of the agonist which could alter
bodily functions and cause toxicity. An inverse agonist is much like taking a placebo as it would have no
therapeutic consequences to the patient and they may as well not even take it; although it can still cause
side or adverse effects (Camprodon & Roffman, 2016).
Compare and contrast the actions of g couple proteins and ion gated channels
Ion channel-linked bind a ligand (can be an anion, cation, or neutral) opening a channel through the
membrane allowing specific ions to pass through. When a ligand binds to the extracellular region of the
channel, a change in the protein’s structure allows ions such as sodium, calcium, magnesium, and
hydrogen to pass through. G-protein-linked receptors bind a ligand activating a membrane protein. The
activated G-protein interacts with either an enzyme in the membrane or an ion channel (Boundless,
2020). G-protein-coupled receptors are the largest protein family, between 600 and 1000, and are known
as seven transmembrane receptors and about 45% of medicinal drugs affect them (G protein-coupled
receptors, 2022).
Explain how the role of epigenetics may contribute to pharmacologic action
Epigenetics is the study of DNA modifications that do not change an individual’s genetic
code but can influence gene expression when certain genes are switched on and off.
Things that affect expression can be exposure to pollutants or an individual’s diet. The
ATP-dependent chromatin remodeling complex BAF is the main area of study in cancer
epigenetics as it is found to be a mutation in one-fifth of all human cancers. Lysine-
specific demethylase 1 (LSD1) showed in an experiment with adult mice that
neurodegeneration and paralysis were present when LSD1 was eliminated leading to
potential research for patients with Alzheimer’s disease as LSD1 plays an essential role
in frontotemporal dementia (Moore, 2020).
Explain how this information may impact the way you prescribe medications to
patients. Include a specific example of a situation or case with a patient in which

the psychiatric mental health nurse practitioner must be aware of the
medication’s action
One must know the mechanism of action and how a drug clears the body, so the patient
does not have serious side or adverse effects. Children, adults, and geriatrics cannot
take the same dose and have the same therapeutic effects. Genetics play an important
role, as well as ethnicity, blood type, and sexual orientation when it comes to certain
pharmaceuticals. Hepatic cytochrome P450 enzyme interactions can induce or inhibit
the metabolism of certain drugs. Approximately 10% of Caucasians are poor
metabolizers of the P450 2D6 enzyme. Thus, taking Bupropion combined with
paroxetine may increase the risk of seizures, which may occur rarely with either
medication. Bupropion can increase the blood levels of paroxetine and may increase
other side effects. Alcohol can enhance effectiveness and should be limited to any
antipsychotics (Drug Interaction Report, 2022).
References

Boundless. (2020, August 14). Types of Receptors. Retrieved 2022, from Biology
LibreTexts: https://bio.libretexts.org/@go/page/13216
Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric Neuroscience: Incorporating
Pathophysiology into Clinical Case Formulation. In T. A. Stern, M. Fava, T. E.
Wilens, & J. F. Rosenbaum, Massachusetts General Hospital
psychopharmacology and neurotherapeutics (pp. 1-9). Elsevier.
CHAPTER 7. (n.d.). In PSYCHIATRIC-MENTAL HEALTH NURSE PRACTITIONER
REVIEW AND RESOURCE MANUAL (4th ed.). Retrieved from
https://www.nursingworld.org/~4ae124/globalassets/catalog/sample-
chapters/pmhnpsamplechapter.pdf
Drug Interaction Report. (2022). Retrieved from Drugs.com Know More. Be Sure. :
https://www.drugs.com/interactions-check.php?drug_list=1800-0,440-0
G protein-coupled receptors. (2022). Retrieved from Molecular Devices:
https://www.moleculardevices.com/applications/g-protein-coupled-receptors#gref
Moore, S. (2020, April 7). What Role Does Epigenetics Play in Drug
Discovery? Retrieved from AZO Life Sciences:
https://www.azolifesciences.com/article/What-Role-Does-Epigenetics-Play-in-
Drug-Discovery.aspx

week 2 discussion

COLLAPSE

1. While working in a drug addiction treatment center we use a variety of
medication assisted treatments, including drugs that are agonists, partial
agonists, and antagonists. Methadone is an opioid agonist
treatment (Renner, Levounis, & LaRose, 2018). An agonist will attach to and
activate opioid receptors, this has a stabilizing effect which prevents
withdrawals, the patient does not have to detox to take the medication, but
will experience withdraw when they stop taking the medication
(Renner, Levounis, & LaRose, 2018). A partial agonist drug for opioid use
disorder includes buprenorphine, these drugs attach to the opioid receptor but
do not simulate them to the same level as a full agonist thus the excessive
stimulation of the dopamine reward system is blocked, patients do not need to
detox to start on the medication but withdrawal symptoms will be felt when the
drug is stopped (Renner, Levounis, & LaRose, 2018). An antagonist drug for
opioid use disorder and alcohol use disorder is naltrexone, which attaches to
the opioid receptor but does not cause a release of dopamine, they create a
barrier that blocks opioid molecules from attaching to the opioid receptors,
therefore patients must detox before starting the medication (Hartwell, et al,
2020).
Another mechanism of drugs is an inverse agonist, as seen in antihistamines.
H1 antihistamines produce the opposite effect on the receptor to histamine
which can produce the therapeutic effect of sleep, thus taking
an antihistamine can be used as a sleep aide since histamine stimulates
wakefulness (Camprodon & Roffman, 2016).
2. Neurotransmitters signals change to post-synaptic neuron function via
receptor and second messenger systems (Camprodon & Roffman, 2016).
These signals result in changes to the neuronal activity, which is often
expressed in changes to gene expression (Camprodon & Roffman, 2016).
Pharmacological intervention targets neurotransmitter receptors which are
usually ion channels but can also be G-protein coupled receptors
(GPCRs) (Camprodon & Roffman, 2016). Ion gated channels have a rapid
effect, they rapidly alter membrane potential and neuronal
activity (Camprodon & Roffman, 2016). GPCRs work via slower messenger
systems which include sequential multi-enzyme cascades which can act as on
– off switches at certain branch points (Camprodon & Roffman, 2016). Certain
antipsychotic drugs such as clozapine and olanzapine block specific GPCRs
that would normally bind to dopamine or serotonin thus alleviating symptoms
of schizophrenia (Rogers, 2019).
3. Epigenetics refers to how our experiences may interact with our gene
function. The code of the gene might not be altered but the function of the

gene is changed, as with abused children (Camprodon & Roffman, 2016).
Child abuse can have long term effects on behavior and cognition, leading to
an altered response to stress due to the dysfunctional programming
hypothalamic – pituitary – adrenal axis (Camprodon & Roffman,
2016). These changes to the chromatic structure can be treated or even
reversed with pharmacologic action, as seen with the use of valproic acid
(Camprodon & Roffman, 2016).
4. Recently, I started working at an addiction and treatment center. There are
various services that we provide including detox, 30-day inpatient beds, and
sober living with outpatient treatment. I work in the outpatient center and see
patients when they usually have a week to thirty days sober, and they are out
of the withdrawal period. Looking back at the patient’s detox chart, they often
receive “comfort medications”, these include the use of clonidine. Clonidine
dampens noradrenergic tone which during opioid withdraw, elicits calming and
sedating effects on the patient (Camprodon & Roffman, 2016). When patients
are using opioids, the drug acts through “G-protein coupled receptors to inhibit
the cAMP system and reduce the activity of locus coeruleus
neurons” (Camprodon & Roffman, p 15, 2016). When the opioids are stopped
hyperactivity of the locus coeruleus starts and the patient develops autonomic
and psychological hyperarousal, clonidine then dampens these symptoms. By
knowing the mechanism of action for this drug it can safely be prescribed to
combat the symptoms of withdrawal based on the knowledge of therapeutic
effect. Before this class, I was not sure of the mechanism of action of
clonidine, this information will make me a better clinician as I can explain to
my patients why an antihypertensive drug also helps
with withdrawal symptoms.

References
Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric neuroscience:
Incorporating pathophysiology into clinical case formulation. In T. A. Stern,
M. Favo, T. E. Wilens, & J. F. Rosenbaum. (Eds.), Massachusetts General
Hospital psychopharmacology and neurotherapeutics (pp. 1–19). Elsevier.
Hartwell, E. E., Feinn, R., Morris, P. E., Gelernter, J., Krystal, J., Arias, A. J.,
Hoffman, M., Petrakis, I., Gueorguieva, R., Schacht, J. P., Oslin, D., Anton, R.
F., & Kranzler, H. R. (2020). Systematic review and meta‐analysis of the
moderating effect of rs1799971 in OPRM1, the mu‐opioid receptor gene, on
response to naltrexone treatment of alcohol use disorder. Addiction, 115(8),
1426–1437. https://doi.org/10.1111/add.14975
Renner, J. A., Jr., Levounis, P., & LaRose, A. T. (2018). Office-based
buprenorphine treatment of opioid use disorder (Second edition.). American
Psychiatric Association Publishing.

Rogers, K. (2019, February 7). G protein-coupled receptor. Encyclopedia
Britannica. https://www.britannica.com/science/G-protein-coupled-receptor

Week 2 Discussion + Oladejo + B (6630)
COLLAPSE

Explain the agonist-to-antagonist spectrum of action of psychopharmacologic
agents, including how partial and inverse agonist functionality may impact the
efficacy of psychopharmacologic treatments.
An agonist is a molecule /compound that can bind to metabotropic and/or
ionotropic receptor, and produces similar response with the receptor site while an
antagonist is a molecule/compound that binds to a target, does not allow other molecules
to bind to it and stops the response of the receptor site (Grandy, 2016).  An inverse
agonist is a molecule/compound that binds to the receptor site and does not allow the
agonist to perform its function by producing a negative effect (Grandy, 2016). A partial
agonist (just as the name sounds) is a molecule/compound that binds to a target and only
has the capacity to partially activate the receptor (Grandy, 2016).
Compare and contrast the actions of g coupled proteins and ion gated channels.
The neurotransmitter signals can change the response of the postsynaptic
membrane through a combination of receptors or second messenger systems. The Ion
gated channels are rapid-effect neurotransmitter receptors (Stern, Fava, Wilen, &
Rosenbaum, 2016). The massive inflow of these ions causes a change in the membrane
potential and the function of the neuron. The G-proteins work through a slower second
messenger system that constitutes various complex enzymatic stages (Stern et al.,
2016).The G -proteins change the activity of numerous target proteins by converting
receptor signals to groups of cellular effects. Examples of such target proteins  are
synaptic proteins that ensure the synapses are effectively performing their functions and
the ion channel that regulates the neuronal activity (Stern et al., 2016).
Explain how the role of epigenetics may contribute to pharmacologic action.
Epigenetics refers to the ability to regulate or change the genetic
expression without changing their order or course (Furtado et al., 2019). For
example in the treatment of cancer, epigenetic drugs (epidrugs) can change the
DNA and chromatin structures and allow the disruption of transcriptional and
post-transcriptional modifications. Epigenetic drugs control the enzymes
necessary for their maintaining and reactivating epigenetically silenced tumor-
suppressor and DNA repair genes (Furtado et al., 2019). Epigenetics play a
major role in the treatment of various diseases. DNA methylation, histone
modifications, and non-coding RNAs are examples of such modifications
from epigenetics (Furtado et al., 2019).

Explain how this information may impact the way you prescribe medications to patients.
Include a specific example of a situation or case with a patient in which the psychiatric
mental health nurse practitioner must be aware of the medication’s action.

The diagnosing and treatment of mental health are evolving. The psychiatric
mental health nurse practitioners (PMHNP) must have a good knowledge of the
relationship between epigenetics medications and various mental health diseases. Having

a solid knowledge of prescribing medications and the molecular effects of the drugs will
yield a better patient outcome. For example, drugs that block the serotonin transporter
(SERT) prolong serotonin’s action (Stern et al., 2016). These drugs are selective
serotonin reuptake inhibitors which are used in the treatment of depression and anxiety
disorders. The discovery of two genetic variants in the SERT gene has played a major
role in psychiatric neuroscience (Stern et al., 2016). The Long variant enhances the
transportation in the synaptic cleft, reduces the duration and intensity of
neurotransmission while the short variant lowers the transportation and increases the
serotonin signaling (Stern et al., 2016). The S-variant is attributed to the cause of
depression and anxiety disorders (Stern et.al, 2016)
References

Furtado et al. (2019). Epidrugs: Targeting epigenetic marks in cancer
treatment. https://doi.org/10.1080/15592294.2019.1640546
Grandy, D.K. (2016) Amphetamine activate G-coupled trace amine associated-related 1
(TAAR1). Neuropathology of drug addictions and substance misuse
Stern, T.A., Fava, M., Wilens, T.E., & Rosenbaum, J.F. (2016). Psychopharmacology and
neurotherapeutics

WEEK 2

COLLAPSE
Psychopharmacologic Approaches
Agonist to Antagonist Spectrum of Action

To achieve better clinical outcomes for patients, one should prescribe accurate and
precise dosages of pharmacologic agents and, at the same time, look out for adverse effects.
Therefore, a proper understanding of psychopharmacology is key for the proper management of
patients. Most psychopharmacologic agents alter neurotransmission by mimicking
neurotransmitter ligands or altering the concentration of neurotransmitters present in the synaptic
cleft. Psychopharmacologic agents are grouped into Full agonist, Partial agonist, antagonist, and
inverse agonists.
Full and Partial Agonists
An agonist is a substance that mimics the endogenous neurotransmitter and binds to a
receptor to produce a desired and similar action as the endogenous neurotransmitter (Papke et
al., 2022). Agonist agents are grouped into full and partial agonists depending on the efficacy
and intrinsic activity. According to Papke et al. (2022), a full agonist is a molecule with a full
affinity to receptors and an intrinsic activity of greater than one. Full agonists have maximum
efficacy. Isoprenaline is an example of a full agonist that mimics adrenaline and binds to
adrenergic receptors.
On the other hand, a partial agonist is a molecule that mimics endogenous ligands with a
full affinity to receptors and an intrinsic activity of between zero and one (Yu et al., 2021). For
example, Pilocarpine is an example of a partial agonist that mimics acetylcholine and binds to
muscarinic cholinergic receptors. According to Jain et al. (2020), Pilocarpine is used in the
management of glaucoma as it lowers intraocular pressure by causing contraction of the ciliary
muscle.
Antagonists and Inverse Agonists
According to Papke et al. (2022), an antagonist is a drug that inhibits the action of
another drug or endogenous ligand by binding to the allosteric site or primary site of the
receptor. Berg and Clarke (2018), reports that antagonists bind to the receptor but do not
activate them, possess affinity, and lack efficacy. Yu et al. (2021), reports that in the absence of
a ligand, a receptor may be completely active or inactive. Activity in the absence of a ligand is
termed constitutive activity. According to Berg and Clarke (2018), an inverse agonist is a drug
that decreases the activity of active receptors to their inactive state. The number of active

receptors is decreased to less than what is observed in the absence of a ligand. Intrinsic activity is
the capacity of an agonist to produce a response.
Additionally, full agonist, which is mirrored by the maximum response, has an intrinsic
activity of one. Therefore, based on the intrinsic activity concept, an inverse agonist has an
intrinsic activity of -1. Flumazenil is an example of an inverse agonist.
G Couple Proteins and Ion Gated Channels

Receptors’ Similarities
G-Protein Coupled Receptors (GPCRs) and ion channel receptors have some
characteristics in common. First, GPCRs and ion channels are bound to the membrane and
present on the cell surface. According to GPCRS is the largest membrane receptor that generates
a response by linking drug-binding at the extracellular part with the intracellular portion of the
cell. Ion channels are transmembrane proteins that allow ion flow when a ligand binds receptors.
Secondly, GPCR and ion channels are activated by binding a ligand.
Receptors’ Differences
GPCRs and Ion channel receptors differ in several ways. First, the receptors found on the
extracellular portion of the GPCRs are chemical ligands while ligands. Secondly, Ion channels
regulate the flow of ions such as Ca 2+  and Na +  while GPCRs do not regulate ion flow. According
to Dolphin et al. (2020), GPCRs cause intracellular signaling by activating a cascade of reactions
from forming an alpha-GTP complex which activates the enzyme adenylate cyclase and initiates
a response. Lastly, GPCRs have a prolonged and extensive duration of effect, while in ion
channels, it is short.

Role of Epigenetics to Pharmacologic Agents

According to Cacabelos et al. (2019), epigenetics are heritable phenotypic changes that
occur without alteration on the primary DNA sequence. Epigenetics are external modifications
that turn “on” and “off” gene expression. Epigenetic changes are caused by environmental
factors such as exposure to drugs and toxins, anxiety, and life stresses, leading to traits that are
passed down for generations. According to Cacabelos et al. (2019), epigenetics causes
modification of the DNA sequence through methylation, acetylation, and histone modification.
The variability of drug efficacy depends on pharmacokinetics and
pharmacodynamics. Cacabelos et al. (2019) report that epigenetic modifications cause
alteration in drug metabolism, transport, and distribution of receptors, affecting drug efficacy.
Codeine is a prodrug that requires the metabolism of morphine by the enzyme CYP2D6 for
activation. A study done by Mostafa et al. (2019), showed that 3.3% of Caucasians lacked the

gene coding for the enzyme CYP2D6. Therefore, the efficacy of codeine in this group of
individuals is compromised; thus should have alternative prescriptions. Additionally, epigenetic
changes may cause mutations in drug receptors, causing the inability of drugs to bind.
Understanding and integrating epigenetics in pharmacological treatment will lead to accurate
prescription and dosages.

Clinical Implications

The knowledge I have learned from understanding the spectrum of agonist and antagonist
in pharmacologic has changed my perspective and given me a broader lens to view how drugs
act. For example, I have fully understood the concept of constitutive and intrinsic activity. In a
clinical situation, I have learned the use of first and second-generation antipsychotics in the
management of schizophrenia. Schizophrenia is a mental disorder caused by an imbalance in
dopamine. Risperidone is a first-generation antipsychotic which acts as an antagonist at the
dopamine receptor. Therefore, risperidone mimics dopamine and prevents dopamine from
binding to the receptor. Additionally, as a PMNHP, I will be on the lookout for side effects
caused by the reduction of dopamine.

References

Mostafa, S., Kirkpatrick, C. M., Byron, K., & Sheffield, L. (2019). An analysis of allele,
genotype, and phenotype frequencies, actionable pharmacogenomic (PGx) variants and
phenoconversion in 5408 Australian patients genotyped for CYP2D6, CYP2C19,
CYP2C9 and VKORC1 genes. Journal of Neural Transmission, 126(1), 5-
18. https://doi.org/10.1007/s00702-018-1922-0
Yu, J., Zhu, H., Lape, R., Greiner, T., Du, J., Lü, W., … & Gouaux, E. (2021). Mechanism of
gating and partial agonist action in the glycine receptor. Cell, 184(4), 957-
968. https://doi.org/10.1016/j.cell.2021.01.026
Berg, K. A., & Clarke, W. P. (2018). Making sense of pharmacology: inverse agonism and
functional selectivity. International Journal of Neuropsychopharmacology, 21(10),
962-977. https://doi.org/10.1093/ijnp/pyy071
Dolphin, A. C., Insel, P. A., Blaschke, T. F., & Meyer, U. A. (2020). Introduction to the theme
“ion channels and neuropharmacology: from the past to the future”. Annual Review of
Pharmacology and Toxicology, 60, 1-6. https://doi.org/10.1146/annurev-pharmtox-
082719-110050

Papke, R. L., Andleeb, H., Stokes, C., Quadri, M., & Horenstein, N. A. (2022). Selective
Agonists and Antagonists of α9 Versus α7 Nicotinic Acetylcholine Receptors. ACS
Chemical Neuroscience. https://doi.org/10.1021/acschemneuro.1c00747
Jain, N., Verma, A., & Jain, N. (2020). Formulation and investigation of pilocarpine
hydrochloride niosomal gels for the treatment of glaucoma: intraocular pressure
measurement in white albino rabbits. Drug delivery, 27(1), 888-
899. https://doi.org/10.1080/10717544.2020.1775726
Cacabelos, R., Cacabelos, N., & Carril, J. C. (2019). The role of pharmacogenomics in adverse
drug reactions. Expert Review of Clinical Pharmacology, 12(5), 407-
442. https://doi.org/10.1080/17512433.2019.1597706
Week 2 Discussion Main Post

COLLAPSE

Explain the agonist-to antagonist spectrum of action of psychopharmacologic agents,
including how partial and inverse agonist functionality may impact the efficacy of
psychopharmacologic treatments.
An agonist is created when a chemical activates a receptor and creates a response from
the body. There are also chemicals which can bind to receptors preventing them from triggering
a response which are antagonist. There are chemicals that are added to the body through
medications which are called partial agonist (Choi & Horner, 2021). When they connect with a
receptor, they activate the receptor. The overall effect is fractional when compared to a full
agonist or an endogenous agonist no matter the amount of the medication given. Medications can
also be added to the body which will cause the chemical to bind to the receptor causing a normal
reaction to be blocked but generating an opposite reaction which is called an inverse
agonist (Berg & Clarke, 2018). As medications are reviewed by providers, it is imperative to
look at the individual patient and determine the best course of action for treatment. They may ask
if the patient needs a full agonist medication or if the partial agonist medication will be
sufficient. The patient may be at end of life and pain severity is extremely high, so the provider
prescribes morphine. The morphine is a full agonist instead of tramadol which is a partial agonist
and is used after surgery for moderate to severe pain. If the patient has been newly diagnosed
with schizophrenia, the choice of the medication for the patient is also very individualized to
improve quality of life. The provider may choose aripiprazole which is a partial agonist
instead of clozapine which is an inverse agonist which requires maintenance blood
draws.
Compare and contrast the actions of g couple proteins and ion gated channels.

Both g-protein couple receptors and ion gated channels are proteins. They are both
incorporated in the membrane, and each is controlled by a stimulus in order to be activated. The
differences are in how each function (Miller & Lappin, 2021). With regard to the g-protein
couple receptor, a neurotransmitter binds with a g-protein receptor. This activates the g-protein
connected to the α subunit causing a cascade event where guanosine diphosphate (GDP)
is switched for guanosine triphosphate (GTP). This also causes a separation of (α, β,
and γ) which brings about the ion channel to open and allows ions to move across the
membrane (Miller & Lappin, 2021). During the cycle, the α subunit splits from the β,
and γ causing a cellular response. Other proteins could also be rendered into action.
The GTP is chemically broken down to GDP and the subunits are recollected to form
the inactive g-protein where the cycle is ready to begin again (Miller & Lappin, 2021). In
contrast, on an ion gated channel receptors are part of the make-up of the ion gated
channel. When a neurotransmitter connects to the ion gated channel that single step
causes the ion gated channel to open and allow ions to cross the membrane (Miller &
Lappin, 2021).
Explain how the role of epigenetics may contribute to pharmacologic action.
Medication enters the body to generate an effect by targeting receptors such as protein
transporters, ion channels, membrane receptors, and enzymes (Szyf, 2017). The end result of the
medication is to cause an action such as lowering an individual’s blood pressure if given
clonidine. When looking at the epigenetics and how it can aid in pharmacologic action, research
shows that epigenetics can be reversed as they are outside the genetic code (Ganesan et al.,
2019). Markers which are classified as being either on or off can be reversed by pharmacological
agents which can cause a restorative state to the body (Szyf, 2017).
Explain how this information may impact the way you prescribe medications to patients.
Include a specific example of a situation or case with a patient in which the psychiatric
mental health nurse practitioner must be aware of the medication’s action.
Through the use of this knowledge presented above, it is crucial to gather as much
information from the patient as possible through both a medical history and a physical, which
includes a physical environmental history for possible exposure of elements. Because new
medications given can be affected by other medications the patient is taking, it essential to verify
their current medications as well as any allergies they may have. If giving a patient an
antipsychotic, it is important to know what adverse reactions could occur (Stroup & Gray, 2018).
The patient should be given an appropriate dose of the medication. If this is the first time giving
the medication, staff should be aware and watch for adverse reactions and extrapyramidal

symptoms (Stroup & Gray, 2018). Staff should be ready to give medication to reverse life-
threatening reactions. Antipsychotics can be beneficial to the patient if they are tolerating the
medication, but if any new medication is given, the patient should be observed for possible
adverse reactions.

References

Berg, K. B., & Clarke, W. P. (2018). Making sense of pharmacology: Inverse agonism and
functional selectivity. The International Journal of Neuropsychopharmacology, 10,
962–977. doi:10.1093/ijnp/pyy071
Choi, J., & Horner, K. (2021). Dopamine agonists. StatPearls.
https://www.ncbi.nlm.nih.gov/books/NBK551686/
Ganesan, A., Arimondo, P. B., Rots, M. G., Jeronimo, C., & Berdasco, M. (2019). The timeline
of epigenetic drug discovery: From reality to dreams. Clinical Epigenetics, 11(174).
doi:10.1186/s13148-019-0776-0
Miller, E. J., & Lappin, S. (2021). Physiology, cellular receptor. StatPearls.
https://www.ncbi.nlm.nih.gov/books/NBK554403/
Stroup, T. S., & Gray, N. (2018). Management of common adverse effects of antipsychotic
medications. World psychiatry : Official Journal of the World Psychiatric
Association (WPA), 17(3), 341-356. doi:10.1002/wps.20567
Szyf, M. (2017). Prospects for medications to reverse causative epigenetic processes in
neuropsychiatry disorders. Neuropsychopharmacology : Official Publication of the
American College of Neuropsychopharmacology,, 42(1), 367-368.
doi:10.1038/npp.2016.219
Week 2 Discussion: Initial post

COLLAPSE

Discussion: Foundational Neuroscience

This post will discuss the agonist-to-antagonist spectrum of action of psychopharmacologic
agents, the actions of g couple proteins and ion gated channels, the role of epigenetics, and how this all
affects the way medications are prescribed. As nurse practitioners we need to know the mechanism of
each medication we prescribe, not just what medication will help our patients. As nurse practitioners we
need to be able to know down to the cellular level what each medication does to the body. Positive
outcomes is what we strive for each and every patient.

Explanation of the Agonist-to-Antagonist Spectrum of Action of Psychopharmacologic Agents &
How Partial and Inverse Agonist Functionality May Impact Efficacy of Psychopharmacologic
Treatments
According to Camprodon & Roffman (2016), medications can act as agonists or antagonists.
According to Rosenthal & Burchum (2021), the probability of an agonist drug is decreased by an
antagonist drug by occupying the receptor cells. There can be spare receptors or receptor reserves
(Camprodon & Roffman, 2016). The reserves have the ability of an agonists and they can produce a
maximum response without occupancy of the whole receptor population due to saturation of post-receptor
signaling mechanisms (Rosenthal & Burchum, 2021). According to Camprodon & Roffman (2016),
antagonists have no inherent effectiveness, but agonists medications have intrinsic efficacy. A partial
agonist’s intrinsic efficacy is less than that of a full agonist and produces a submaximal reaction (Berg &
Clark, 2018).
Comparison & Contrast of the g Couple Proteins & Ion Gated Channels
According to Li et al. (2014), G proteins interact with ion channel receptors and this increases the
capacity of neuronal signaling cascades. The nervous system signals allowing rapid chemical
neurotransmitters to message with ionotropic receptors due to the ion gated receptors (Li et al., 2014).
Ion gated channels include GABA, ATP, AMPA, NMDA, nicotine, acetylcholine, glutamate, and glycine (Li
et al., 2014). Li et al., 2014 stated that the g protein and ion gated proteins represent a target for the
therapeutic intervention in neuropsychiatric disorders.
The Role of Epigenetics May Contribute to Pharmacologic Action
According to Camprodon & Roffman (2016), epigenetic are altered by things such as nutrition and
the environment. Epigenetics focus on the modification of genes. Not all patients respond to certain
conditions so special treatments are needed. A patient’s genome information can be used for making
decisions for individual health. Modifying genes helps to treat chronic illness and disease.
Pharmacogenomics works to form a medicine plan that is individualized per patient. DNA methylation is a
type of epigenetic modification that is used by cells to control the gene expression. The DNA segment is
changed in this process but not the sequence of the DNA (Moore et al., 2013). The methyl groups are
added to the DNA molecules. The DNA methylation affects the chromatin structure by inhibiting the gene
expression (Moore et al., 2013). Methylation of cystosines in the DNA is involved in regulating the
chromatin structure (Moore et al., 2013). Dna methylation regulated the gene expression by recruiting
proteins in the gene repression or by inhibiting the binding of transcription factor to the DNA (Moore et al.,
2013).
The Impact of Information Used When Prescribing Medications

When a nurse practitioner is prescribing medications, they must take into consideration all factors
about the patient and their medical history. A patient who is diagnosed as being bipolar  depression may
be prescribed Latuda, but if the patient is Autistic and has bipolar depression Latuda may not be the
medication due to a different gene makeup and they may need a combination of Risperdal and Abilify.
Pharmacogenomics plays a large role in what medication and for who.
In summary, knowing our patients, their medical history, and their overall needs plays a factor in
reaching a positive outcome when prescribing medications. The nurse, the NP, the patient, and the doctor
all are key players in prescribing the correct medications. Overall though, the one signing the prescription
is the one going to be held accountable.

References

Berg, K. A., & Clarke, W. P. (2018). Making sense of pharmacology: Inverse agonism and functional
selectivity.https://doi.org/10.1093/ijnp/pyy071
Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric neuroscience: Incorporating pathophysiology into
clinical case formulation. In T. A. Stern, M. Favo, T. E. Wilens, & J. F. Rosenbaum.
(Eds.), Massachusetts General Hospital psychopharmacology and neurotherapeutics (pp. 1–19).
Elsevier.
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. https://doi.org/10.3389/fncel.2014.00125
Moore, L. D., Le, T., & Fan, G. (2013). DNA methylation and its basic function.
https://doi.org/10.1038/npp.2012.112
practice providers. St. Louis, MO: Elsevier.
Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced

Important information for writing discussion questions and participation

Hi Class,

Please read through the following information on writing a Discussion question response and participation posts.

Contact me if you have any questions.

Important information on Writing a Discussion Question

  • Your response needs to be a minimum of 150 words (not including your list of references)
  • There needs to be at least TWO references with ONE being a peer reviewed professional journal article.
  • Include in-text citations in your response
  • Do not include quotes—instead summarize and paraphrase the information
  • Follow APA-7th edition
  • Points will be deducted if the above is not followed

Participation –replies to your classmates or instructor

  • A minimum of 6 responses per week, on at least 3 days of the week.
  • Each response needs at least ONE reference with citations—best if it is a peer reviewed journal article
  • Each response needs to be at least 75 words in length (does not include your list of references)
  • Responses need to be substantive by bringing information to the discussion or further enhance the discussion. Responses of “I agree” or “great post” does not count for the word count.
  • Follow APA 7th edition
  • Points will be deducted if the above is not followed

Welcome to class

Hello class and welcome to the class and I will be your instructor for this course. This is a -week course and requires a lot of time commitment, organization, and a high level of dedication. Please use the class syllabus to guide you through all the assignments required for the course. I have also attached the classroom policies to this announcement to know your expectations for this course. Please review this document carefully and ask me any questions if you do. You could email me at any time or send me a message via the “message” icon in halo if you need to contact me. I check my email regularly, so you should get a response within 24 hours. If you have not heard from me within 24 hours and need to contact me urgently, please send a follow up text to.

I strongly encourage that you do not wait until the very last minute to complete your assignments. Your assignments in weeks 4 and 5 require early planning as you would need to present a teaching plan and interview a community health provider. I advise you look at the requirements for these assignments at the beginning of the course and plan accordingly. I have posted the YouTube link that explains all the class assignments in detail. It is required that you watch this 32-minute video as the assignments from week 3 through 5 require that you follow the instructions to the letter to succeed. Failure to complete these assignments according to instructions might lead to a zero. After watching the video, please schedule a one-on-one with me to discuss your topic for your project by the second week of class. Use this link to schedule a 15-minute session. Please, call me at the time of your appointment on my number. Please note that I will NOT call you.

Please, be advised I do NOT accept any assignments by email. If you are having technical issues with uploading an assignment, contact the technical department and inform me of the issue. If you have any issues that would prevent you from getting your assignments to me by the deadline, please inform me to request a possible extension. Note that working fulltime or overtime is no excuse for late assignments. There is a 5%-point deduction for every day your assignment is late. This only applies to approved extensions. Late assignments will not be accepted.

If you think you would be needing accommodations due to any reasons, please contact the appropriate department to request accommodations.

Plagiarism is highly prohibited. Please ensure you are citing your sources correctly using APA 7th edition. All assignments including discussion posts should be formatted in APA with the appropriate spacing, font, margin, and indents. Any papers not well formatted would be returned back to you, hence, I advise you review APA formatting style. I have attached a sample paper in APA format and will also post sample discussion responses in subsequent announcements.

Your initial discussion post should be a minimum of 200 words and response posts should be a minimum of 150 words. Be advised that I grade based on quality and not necessarily the number of words you post. A minimum of TWO references should be used for your initial post. For your response post, you do not need references as personal experiences would count as response posts. If you however cite anything from the literature for your response post, it is required that you cite your reference. You should include a minimum of THREE references for papers in this course. Please note that references should be no more than 5 years old except recommended as a resource for the class. Furthermore, for each discussion board question, you need ONE initial substantive response and TWO substantive responses to either your classmates or your instructor for a total of THREE responses. There are TWO discussion questions each week, hence, you need a total minimum of SIX discussion posts for each week. I usually post a discussion question each week. You could also respond to these as it would count towards your required SIX discussion posts for the week.

I understand this is a lot of information to cover in 5 weeks, however, the Bible says in Philippians 4:13 that we can do all things through Christ that strengthens us. Even in times like this, we are encouraged by God’s word that we have that ability in us to succeed with His strength. I pray that each and every one of you receives strength for this course and life generally as we navigate through this pandemic that is shaking our world today. Relax and enjoy the course!

Did you find apk for android? You can find new Free Android Games and apps.