Discussion: Foundational Neuroscience
As a psychiatric nurse practitioner, it is essential for you to have a strong background in foundational neuroscience. In order to diagnose and treat patients, you must not only understand the pathophysiology of psychiatric disorders but also how medications for these disorders impact the central nervous system. These concepts of foundational neuroscience can be challenging to understand. Therefore, this Discussion is designed to encourage you to think through these concepts, develop a rationale for your thinking, and deepen your understanding by interacting with your colleagues.
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For this Discussion, review the Learning Resources and reflect on the concepts of foundational neuroscience as they might apply to your role as the psychiatric mental health nurse practitioner in prescribing medications for patients.
By Day 3 of Week 2
Post a response to each of the following:
- 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.
- Compare and contrast the actions of g couple proteins and ion gated channels.
- Explain how the role of epigenetics may contribute to pharmacologic action.
- 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.
Read a selection of your colleagues’ responses.
By Day 6 of Week 2
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.
Note: For this Discussion, you are required to complete your initial post before you will be able to view and respond to your colleagues’ postings. Begin by clicking on the “Post to Discussion Question” link and then select “Create Thread” to complete your initial post. Remember, once you click on Submit, you cannot delete or edit your own posts, and you cannot post anonymously. Please check your post carefully before clicking on Submit!
Neuroscience Overview
Psychopharmacological treatment effects come from the alteration of neurotransmitter binding in the synapse through several types of actions. Agonism is when neurotransmitters are made more available to the postsynaptic cell. This can be done by stimulating synthesis or release of the transmitter, and also by blocking the reuptake or breakdown (Caprodon & Roggman, 2016). Antagonism is when a drug binds to a receptor but does not cause any action. The outcome of this is that other agents cannot bind to those same receptors and activate the associated response (Salahudeen & Nishtala, 2017). Partial agonists bind to and stimulate action on some but not all available receptors. In inverse agonism, a drug binds to the receiving cell but causes the opposite of the cell’s intended effect (Salahudeen & Nishtala, 2017).
Once there is an activation of a receptor at the postsynaptic neuron, communication can occur in various ways. Two examples are ion gated channels and G-protein coupled receptors (GPCRs) (Caprodon & Roggman, 2016). The activation of ion gated channels can alter the electrical potential of a neuron at the level of the cell membrane and cause relatively quick effects. In contrast, activated GPCRs have more complicated effects that alter the cell via a series of sequential steps and take longer for their intended effect (Caprodon & Roggman, 2016).
Epigenetics in psychiatry is the study of how identifiable biological/genetic predispositions of the individual interact with environmental experiences to cause mental health symptom expression (Caprodon & Roggman, 2016). While pharmacological treatment can be more challenging as a result of these interactions, it can also be used to balance out or correct dysfunctional neuronal pathways (Caprodon & Roggman, 2016).
Clinical Implications
Understanding the above drug functionality can allow for more precision when prescribing psychopharmacological agents. Medications can be utilized to increase or decrease the actions of cells and stimulate or block certain responses based on a patient’s specific symptoms. This knowledge is also essential when moderating the side effects of medication interventions (Delacretaz et al., 2019). An example of how this all comes together would be for a person being treated with antipsychotic medications. Some intended effects come from antagonism of D2 receptors (Caprodon & Roggman, 2016), however, this same action in the hypothalamus often produces increased appetite, weight gain, and long-term metabolic changes (Delacretaz et al., 2019). Some people have also been found to have a genetic variation that increases their risk of this particular negative outcome if they are prescribed antipsychotic medications (Delacretaz et al., 2019). Prescribers with this knowledge must be cautious in prescribing and vigilant for weight gain early in treatment.
References
Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric neuroscience: Incorporating pathophysiology into clinical case formulation. Massachusetts General Hospital Psychopharmacology and Neurotherapeutics. Elsevier.
Delacrétaz, A., Glatard, A., Dubath, C., Gholam-Rezaee, M., Sanchez-Mut, J. V., Gräff, J., von Gunten, A., Conus, P., & Eap, C. B. (2019). Psychotropic drug-induced genetic-epigenetic modulation of CRTC1 gene is associated with early weight gain in a prospective study of psychiatric patients. Clinical Epigenetics, 11(1), 1.
Salahudeen, M. S., & Nishtala, P. S. (2017). An overview of pharmacodynamic modelling, ligand-binding approach and its application in clinical practice. Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 25(2), 165–175. https://doi.org/10.1016/j.jsps.2016.07.002