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Response # 1
Monsurat,
Thank you for a detailed first-week post concerning the introduction to neuroscience. The
first topic this week required in-depth insight and research. I particularly found the information
regarding epigenetics to be very interesting during my learning. In your post, you mentioned that
epigenetic mechanisms influence the transcription of DNA modifying access to the DNA
sequence. In addition, it is important to understand that the epigenetic mechanism that regulates
both the function and structure of chromatin will facilitate modifications in the expressions of
genes as an effect of different stimulus (Vialou, Feng, Robinson, & Nestler, 2013). Stahl (2013),
also re-iterates how the regulation of epigenetics over gene expression or silencing is achieved
by altering structures of chromatin. The epigenetic control of silencing or expressing gene
modification is a structure of chromatin, which is achieved through chemicals such as
methylation, phosphorylation, acetylation, and methods such as neurotransmission, the
environment, and drugs (Stahl, 2013).
Moreover, you mentioned the key points regarding the epigenetic regulation of brain
functions in causing psychiatric disorders, and the effectiveness of the epigenetic regulation of
brain derive neutrophic factors genes of depression. The insight you have included influenced
further my understanding of how epigenetics works on these genes. For instance, brain-derived
neurotrophic factor (BDNF) is critical in brain development and neuron regeneration, which
abnormalities have been noted in numerous neurological diseases one being Alzheimer’s disease
(AD) (Chen & Chen, 2017). So based on this information, epigenetics is considered as either a
turning on or off of a gene, which consider Alzheimer’s as a set of genes that do play a role in
the disease process, but does not mean that genes actually cause the disease (Fenogilo, Scarpini,
Serpente, & Galimberti, 2018). Epigenetics is developing as a link missing among brain health,
with specific changes in nucleic acids or their associated proteins causing differential patterns of
gene activation that will favor either cognitive enhancement or cognitive loss. Increasing
epigenetic signaling is appearing as a significant risk factor for illnesses of aging, including
neurodegeneration and AD (Fenogilo, Scarpini, Serpente, & Galimberti, 2018).
References:
Chen, K-W., & Chen, L. (2017). Epigenetic Regulation of BDNF Gene during Development and
Diseases.;International Journal of Molecular Sciences, Vol 18, Iss 3, p 571 (2017), (3), 571.
https://doi-org.ezp.waldenulibrary.org/10.3390/ijms18030571
Fenoglio, C., Scarpini, E., Serpente, M., & Galimberti, D. (2018). Role of genetics and
epigenetics in the pathogenesis of Alzheimer’s disease and frontotemporal dementia.;Journal of
Alzheimer’s Disease,;62(3), 913–932. https://doi-org.ezp.waldenulibrary.org/10.3233/JAD-
170702
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
Vialou, V., Feng, J., Robinson, J., & Nestler, E. J. (2013). Epigenetic Mechanisms of Depression
and Antidepressant Action.;Annual Review of Pharmacology and Toxicity, 53(1), 59-87.
Response #2
Pamela,
Your post was very interesting this week, and you provided a detailed example regarding
agonist to antagonist spectrum in a person addicted to nictonie. In addition to your post, I would
also like to include that in regards to the psychopharmacologic agents, the defining factors
between an agonist and an antagonist drug is determined based on how they interact with
neurotransmitters. G- protein-coupled brain receptors have proven to provide numerous targets
for psychotropic drugs and have been explored through brain imaging (Zimmer, 2016). Drugs
that interact with receptors can be classified therefore, as being either agonists or antagonists,
which have either direct or indirect binding (New Health Guide, n.d.). Drugs can directly act to
bind to neurotransmitter sites and produce the same display as full agonists (Stahl, 2013). Drugs
can indirectly act to boost the levels of natural full agonist, which occurs after inactive
neurotransmitters are blocked (Stahl, 2013). Stahl (2013), expounds on how indirect agonist
inhibit monoamine transporters such as SERT and DAT, or by blocking acetylcholinesterase and
monoamine oxidase enzyme destruction of neurotransmitters (Stahl, 2013).
Stahl (2013), also describes two major ways to stimulate G-protein-linked receptors, with
full agonist and antagonist actions that include directly and indirectly bind. Those two points that
you have included; however, I would like to focus on the antagonist. The antagonist drugs work
by inhibiting the brains neurotransmitters, which also work with two types which are direct-
acting and indirect-acting antagonist (Health Guide, n.d.). Furthermore most
radiopharmaceuticals develop to target specific receptors that are pharmacologically, antagonists;
however, pharmacological studies show that antagonists bind to both G-protein coupled
receptors and to non-functional receptors of the same family (Zimmer, 2016). However, agonists,
bind only to functioning G-protein-coupled receptors (Zimmer, 2016). Therefore, direct-acting
antagonist work by occupying the presence on receptors, which would usually have
neurotransmitters present to inhabit the site, and indirect work by preventing neurotransmitters to
release on the receptor sites (Zimmer, 2016).
References:
New Health Guide. (n.d.). Agonist vs. Antagonist Drug: Differences to know. Retried from
http://www.newhealthguide.org/Agonist-Vs-Antagonist.html
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
Zimmer, L. (2016). Pharmacological agonists for more-targeted CNS radio-
pharmaceuticals.;Oncotarget,;7(49), 80111-80112.
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