Our cells are filled with intracellular and surface cell receptors (Berg & Clarke, 2018).  These receptor proteins are delineated by structure and bind to a variety of substances responsible for creating a reaction or lack thereof. When a ligand binds to the appropriate receptor, signal transduction activates the receptor and produces a biological response ( Berg & Clarke, 2018).  Changes in shape or activity after binding allow signal transmission outside the cell or significant changes within the cell, creating an altered chemical when binding to a ligand-gated-ion channel ( Berg & Clarke, 2018). This post will discuss the agonist/ antagonist spectrum of psychopharmacological agents, G-proteins and ion-gated channels, and epigenetics and their relevance to practice.  Agonists act like ligands, binding to receptors and causing action (Berg & Clarke, 2018).  Ligands or agonists consist of pharmaceuticals, drugs, light, hormones, and nerve impulses. Ligands and agonists jump in and out of receptors, increasing signaling or changes in the cell.  Antagonists block the standard action of ligands, preventing a response from the receptor (Berg & Clarke, 2018).  Competitive antagonists bind to receptors and prevent ligands from attaching to its preferred receptor, inhibiting stimulation, and leaving the receptor unchanged (Berg & Clarke, 2018).  Naloxone is a competitive antagonist to opiate receptors London, 2017).  The naloxone has a stronger affinity for the receptor, making it more desirable.  The medication discontinues the effects of the opiates by taking their place on the receptor. The higher the dose of opiates circulating the more naloxone required. Due to the excess amount of continued competition for receptors, some patients require multiple doses of naloxone before regaining the ability to breath or regain consciousness (London, 2017).  G-protein coupled receptors (GPCRs) target 30-50% of psychotropic medications (Stahl, 2013).  As the most abundant protein family, GPCR ligands include neurotransmitters such as serotonin, norepinepherine, and dopamine. After  aligand binds to a GPCR, the GPCR undergoes a conformational change (London, 2017).  Alpha subunit exchanges Guanyl nucleotide phosphates, GTP, GPP, and Alpha unit disassociates and regulates target proteins (London, 2017).  Regulation of neurotransmission is imperative in medication management (London, 2017).  The target proteins can then relay signals via a second messenger, and GTP is finally hydrolyzed to GPP (Lambert, 2004). G-protein receptors tend to have a delay in effect due to a requirement for the accumulation of changed cellular function (London, 2017).   Ion gated channel linked receptors open and close in response to a chemical message changing signal transduction in the synaptic cleft. These ion channels act like pores in the cellular membrane to allow ion passage (Stahl, 2013).  Transmembrane ion channels open and close in response to the binding of a ligand, dif.

1. Our cells are filled with intracellular and surface cell receptors
(Berg & Clarke, 2018). These receptor proteins are delineated
by structure and bind to a variety of substances responsible for
creating a reaction or lack thereof. When a ligand binds to the
appropriate receptor, signal transduction activates the receptor
and produces a biological response ( Berg & Clarke, 2018).
Changes in shape or activity after binding allow signal
transmission outside the cell or significant changes within the
cell, creating an altered chemical when binding to a ligand-
gated-ion channel ( Berg & Clarke, 2018). This post will
discuss the agonist/ antagonist spectrum of
psychopharmacological agents, G-proteins and ion-gated
channels, and epigenetics and their relevance to practice.
Agonists act like ligands, binding to receptors and causing
action (Berg & Clarke, 2018). Ligands or agonists consist of
pharmaceuticals, drugs, light, hormones, and nerve impulses.
Ligands and agonists jump in and out of receptors, increasing
signaling or changes in the cell. Antagonists block the standard
action of ligands, preventing a response from the receptor (Berg
& Clarke, 2018). Competitive antagonists bind to receptors and
prevent ligands from attaching to its preferred receptor,
inhibiting stimulation, and leaving the receptor unchanged
(Berg & Clarke, 2018). Naloxone is a competitive antagonist to
opiate receptors London, 2017). The naloxone has a stronger
affinity for the receptor, making it more desirable. The
medication discontinues the effects of the opiates by taking
their place on the receptor. The higher the dose of opiates
circulating the more naloxone required. Due to the excess
amount of continued competition for receptors, some patients
require multiple doses of naloxone before regaining the ability
to breath or regain consciousness (London, 2017).
G-protein coupled receptors (GPCRs) target 30-50% of
psychotropic medications (Stahl, 2013). As the most abundant

2. protein family, GPCR ligands include neurotransmitters such as
serotonin, norepinepherine, and dopamine. After aligand binds
to a GPCR, the GPCR undergoes a conformational change
(London, 2017). Alpha subunit exchanges Guanyl nucleotide
phosphates, GTP, GPP, and Alpha unit disassociates and
regulates target proteins (London, 2017). Regulation of
neurotransmission is imperative in medication management
(London, 2017). The target proteins can then relay signals via a
second messenger, and GTP is finally hydrolyzed to GPP
(Lambert, 2004). G-protein receptors tend to have a delay in
effect due to a requirement for the accumulation of changed
cellular function (London, 2017).
Ion gated channel linked receptors open and close in response to
a chemical message changing signal transduction in the synaptic
cleft. These ion channels act like pores in the cellular membrane
to allow ion passage (Stahl, 2013). Transmembrane ion
channels open and close in response to the binding of a ligand,
differentiated by shape. The binding will cause the channel to
open or close, changing the protein conformation of the entire
structure (Berg & Clarke, 2018). When channels open, ions like
potassium, sodium, chloride, and calcium can travel through and
change the electrical process creating an intracellular electrical
response (Berg & Clarke, 2018). Psychopharmacology relies
heavily on these ion channels in medication management. Ion-
channel linked receptors act along an agonist spectrum;
medications can produce conformational changes in these
receptors to create any state of the agonist spectrum (Stahl,
2013).
The genetic material in the body is referred to as a genome
(Stahl, 2013). Every cell in the body carries the same DNA but
only expresses specific genes required for its domain (Stahl,
2013). For this reason, cells in the dermis only produce cells
required to maintain and rejuvenate the dermis. Epigenetics is
the reason why skin cells differ from brain cells or cardiac

3. cells. Epigenetics is a term used for the external modifications
to the DNA affecting the way it is recognized by cells (Stahl,
2013). There are thee different methods of epigenetics, DNA
myelination, histone acetylation, and microRNA (Stahl, 2013).
Genomes are affected by different exposures during
development, environmental chemicals, drugs or
pharmaceuticals, aging, and diet (Stahl, 2013). Alterations in
genes may result from these exposures and be passed on to
offspring causing a change in the epigenome (Stahl, 2013).
Psychotropic medications target specific molecular sites to
increase neurotransmission. After neurotransmitters release
from neurons, they are quickly recollected and utilized again for
neurotransmission (Stahl, 2013). The five essential sites of
action for psychotropic medications are 12-transmembrane-
region transporter, 7-transmembrane-region-G-protein linked,
enzymes, 4-transmembrane-region-ligand-gated ion channel,
and 6-transmembrane-region-voltage-gated ion channels (Stahl,
2013).
When cellular alterations occur due to brain injury,
neurodegeneration, changes in the extracellular matrix, and
changes in voltage and ligand-gated ion channels transpire (Iori,
2018). A variety of molecular changes, regulation of gene
expression, and epigenetic modifications take place as well(Iori,
2018). As a result, functional impairments such as epilepsy,
developmental delay, cognitive/sensory-motor deficits, and drug
refractoriness may occur (Iori, 2018). Many factors affect the
outcomes of medication. Through assessment is required to
determine environmental issues, incidents of trauma, and
relevant health history. Understanding that many factors
influence the effectiveness of the psychotropic medication is
imperative when determining the appropriate treatment course
(Lambert, 2004).
Recreational drug use, in combination with prescription

4. medication, is critical to determine. Like antidepressants, drugs
like methylphenidate and cocaine target monoamine
transporters; this increases the risk for an oversaturation of
serotonin, norepinephrine, or dopamine in the synaptic cleft.
Oversaturation can potentially cause an issue for signal
transduction in other neurotransmitters (Stahl, 2013). This
oversaturation of serotonin may cause a toxic level of serotonin,
referred to as serotonin syndrome. Patients with serotonin
syndrome/toxicity present with neuromuscular, autonomic, and
mental status changes. Stopping drugs that target monoamine
transporters will help decrease levels of serotonin and should
return the individual to their normal state of health (Foong,
Grindrod, Patel, & Kellar, 2018).
In conclusion, neurotransmission is the cornerstone of
psychopharmacology. Although enormously complicated, it is
imperative providers understand that small changes in cellular
function, additional drugs present in the body, and electrolyte
imbalances affect prescription medication functions and desired
effects. With a shortage of psychiatric prescribers and a mental
health crisis around the world, all healthcare providers must
have a proper understanding of psychopharmacology and
interactions with other body systems.
References
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
Foong, A. L., Grindrod, K. A., Patel, T., & Kellar, J. (2018).
Demystifying serotonin syndrome (or
serotonin toxicity

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Canadian family physician Medecin de famille canadien
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(10), 720–727.
Iori, V. (2018). Epigenetic and pharmacological targeting of
neuroinflammation as novel therapeutic interventions for
epilepsy. Retrieved from
https://hdl.handle.net/11245.1/98bfe10f-44d2-4f42-bc1b-
2f3e605c3ece
Lambert, D. G. (2004). Drugs and receptors,
Continuing Education in Anaesthesia Critical Care & Pain
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(6), 181–184, https://doi.org/10.1093/bjaceaccp/mkh049
London, E. D. (2017).
Imaging drug action in the brain
. Place of publication not identified: Routledge.
Stahl, S. M. (2013). Stahl’s essential psychopharmacology:
Neuroscientific basis and practical applications (4th ed.). New
York, NY: Cambridge University Press