Discussion: Foundational Neuroscience

Respond to at least two of your colleagues on two different days in one of the following ways:

If your colleagues’ posts influenced your understanding of these concepts, be sure to share how and why. Include additional insights you gained.

If you think your colleagues might have misunderstood these concepts, offer your alternative perspective and be sure to provide an explanation for them. Include resources to support your perspective.


Students post:

The agonist to antagonist spectrum of action includes the agonist, the partial agonist, the antagonist, a partial inverse agonist, and finally an inverse agonist. Agonists are neurotransmitters that occur naturally, and they stimulate receptors; they also open the channel completely and allow the maximum amount of frequency allowed. Some drugs are able to work as neurotransmitters are able to stimulate receptors to create a response and these drugs are called agonists. Antagonists are drugs that block the action of a neurotransmitter at the receptor and do not have a specific action in the absence of an agonist. Antagonists work in the channel by retaining their resting state and opening infrequently. It is important to note that antagonists are capable of blocking anything in the agonist spectrum and this includes the inverse agonists. Inverse agonists are drugs that perform in the opposite way of agonists and are more like the exact opposite of agonists. Inverse agonists place the channel into a closed and inactive state. Partial agonists work to activate receptors, but they are not able to create the maximum possible response from the receptor. Partial agonists can sometimes slightly block the effect of an agonist and this is why they are called agonist-antagonist drugs. They work in the channel by increasing the amount of channel opening and the degree of opening. An example is Abilify; this medication works to block brain receptors where the dopamine levels are high and in turn, it decreases the amount of dopamine, which is the desired effect. If dopamine levels are low, then Abilify works to increase the amount of dopamine where it is needed.

G coupled proteins are structured as 7 transmembrane regions. Each region has a core that they cluster around, and the core provides a site for binding the neurotransmitter. Drugs are able to interact with the core or at other places on the receptor and they interact with a large variety of proteins. They are formed by a single polypeptide and cover the membrane and ion channels are made of pores. The pores of the ion channels are able to open and close at the ligand-binding site. Ion channels regulate the flow of ions. A final difference is that G proteins use GTP and ion channels do not.

Epigenetics involves the idea that the function of a gene may evolve without there being a specific change in its code. It is also believed that this change in gene function can be inheritable. The action that typically occurs is either mimicking, blocking, and it’s done either partially or fully. The metabolism of a drug can be affected by changes in gene expression. Epigenetic regulation does not require changes in the DNA.

Epigenetic mechanisms have been studied extensively and it is proven that it contributes to the differential expression of drug-metabolizing genes. This means that we should be careful with the epigenetic properties of drugs. This is because it could affect gene expression and drug disposition. It is possible for drugs to alter the epigenetic signatures of the drug-metabolizing genes and this could lead to unexpected results. An example is an anti-seizure medication and Valproic acid; they are histone deacetylase inhibitors with a potent antitumor mechanism. So, these changes in results should be taken into account when prescribing the medications. It is important to be knowledgeable about the action of medications because they need to know how effective the medication is short and long term. Starting a patient on medication, like Latuda, can change the quality of a patient’s life greatly, and the sooner this is started the faster it may make a difference. However, if this is the wrong kind of medication for the patient it can cause more harm than good. For instance, Latuda can increase suicidal thoughts and may have the opposite therapeutic response and increase anxiety in some people. Latuda is meant to help stabilize emotions and decrease anxiety and agitation.



Kalozoumi, G., Tzimas, C., & Sanoudou, D. (2012). The expanding role of epigenetics. Global Cardiology Science and Practice, 2012(1), 7. https://doi.org/10.5339/gcsp.2012.7

Nutt, D., & Lingford-Hughes, A. (2007). Key concepts in psychopharmacology. Psychiatry, 6(7), 263–267. https://doi.org/10.1016/j.mppsy.2007.05.002

Peng, L., & Zhong, X. (2015). Epigenetic regulation of drug metabolism and transport. Acta Pharmaceutica Sinica B, 5(2), 106–112. https://doi.org/10.1016/j.apsb.2015.01.007

Stahl, S. M. (2013). Ion channels as targets of psychopharmacological drug action. In Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed., pp. 143–199). Cambridge University Press.

A separate question in post:

  1.  How do partial and inverse agonist functionality impact the efficacy of psychopharmacologic treatments?
  2. Can SSRIs cause insomnia? Please discuss.

Answer to this question I got chosen for only needs to be a few sentences, maybe a small paragraph but not part of the above post.

All told, nothing should go over one page if it doesn’t need to.

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Foundational Neuroscience: discussion response

An agonist-antagonist spectrum characterizes psychopharmaceuticals target neurotransmission locations and their aftereffects. Agonists comprise drugs that activate receptors to elicit a reaction, whereas antagonists impede neurotransmission generation (Depoortère et al., 2021). G-protein coupled receptors, ligand-gated ion channels, enzyme-linked receptors, and nuclear receptors are the four basic types of receptors involved in drug-receptor interaction. Agonist interaction promotes ligand-gated ion channel opening, whereas antagonist binding promotes ligand-gated ion channel closure. While agonist is typically understood to induce a response, inverse agonist activities on ligand-gated ion channels are the opposite of full agonist. Given this variability, prescribing drugs necessitates understanding the drug’s agonist and antagonist spectrum (Park et al., 2019).

Epigenetics studies changes in gene expression that occur without a change in the DNA sequence (Feinberg, 2018). Its notion is critical in understanding the function of genes in disease development, neurodegenerative illnesses such as Alzheimer’s, and treatment outcomes. Since many illnesses based on specific genomic profiles are frequently unsuccessfully treated with standard therapy, understanding epigenetics enables the development of personalized medicine.


Feinberg, A. P. (2018). The key role of epigenetics in human disease prevention and mitigation. New England Journal of Medicine, 378(14), 1323-1334.

Park, C., Rosenblat, J. D., Brietzke, E., Pan, Z., Lee, Y., Cao, B., … & McIntyre, R. S. (2019). Stress, epigenetics and depression: a systematic review. Neuroscience & Biobehavioral Reviews, 102, 139-152.

Depoortère, R., Auclair, A. L., & Newman-Tancredi, A. (2021). NLX-101, a highly selective 5-HT1A receptor biased agonist, mediates antidepressant-like activity in rats via prefrontal cortex 5-HT1A receptors. Behavioural Brain Research, 401, 113082.


  1. How partial and inverse agonist functionality impact the efficacy of psychopharmacologic treatments?
  2. Can SSRI’s cause insomnia?

The inverse agonist acts on the same receptor as the agonist but has the opposite effects. Unlike full agonist, inverse agonist has negative efficacy. This is because it “locks” receptors in an inactive state and lowers baseline receptor activity (Bdioui et al., 2018) .

On the other hand, a partial agonist has a lesser intrinsic efficacy (intermediate) than a full agonist, culminating in a submaximal response. The partial agonist functions as an antagonist, competing with the full agonist for active sites. Yes! SSRIs can cause insomnia. This is due to its tendency to cause or worsen sleep bruxism and disrupt muscle tone modulation during REM sleep (Fasipe, 2018).


Fasipe, O. J. (2018). Neuropharmacological classification of antidepressant agents based on their mechanisms of action. Archives of Medicine and Health Sciences, 6(1), 81.

Bdioui, S., Verdi, J., Pierre, N., Trinquet, E., Roux, T., & Kenakin, T. (2018). Equilibrium assays are required to accurately characterize the activity profiles of drugs modulating Gq-protein-coupled receptors. Molecular pharmacology, 94(3), 992-1006.