Please reply to the 2 peer posts using APA format
Post 1
- Discuss the amygdala’s role in anxiety.
- Compare and contrast how fear and worry are thought to be regulated.
- Based on any required lecture material in Module 5, write two possible quiz/exam questions. You may write multiple choice questions or short essay questions. Please include the answer, a rationale, and the source. The questions should be appropriately challenging and must be original (you may not use questions that are on NEI’s website or located online)
The Amygdala’s Role of and Regulation of Anxiety
The amygdala has connections, anatomically, that permit integration of sensory and cognitive information, provoking a fear response when determined appropriate (Stahl, 2021). According to lecture material (NKU, 2024), the amygdala has arousal receptors which increase CREB in the nucleus via norepinephrine and dopamine, as well as glutamate stimulating CREB in the central nuclei of the amygdala. Emotional regulation areas of the prefrontal cortex, specifically the orbitofrontal cortex and the anterior cingulate cortex are thought to have reciprocal connections that regulate fear and stimulate endocrine reactions, secondary to connectivity with the hypothalamus, leading to changes in the hypothalamic-pituitary-adrenal (HPA) axis triggering cortisol level changes (Stahl, 2021). Anxiety is a normal emotional response to fear, however, in excess, fear and anxiety become the core symptoms of anxiety disorders (Stahl, 2021). Chronic levels of elevated cortisol brought on by serial threats, such as those in adverse childhood experiences, are associated with significant comorbidities of impairments in social functioning and mental health (Tzouvara, 2023) as well as physical health, such as coronary artery disease, type 2 diabetes and stroke (Stahl, 2021). The autonomic nervous system responds to fear with responses in cardiovascular responses mediated by pathways between the amygdala and the locus coeruleus (Stahl, 2021). Chronic and inappropriate or serial triggering, as such in anxiety, can lead to these medical comorbidities and anxiety can also be triggered by memories held in the hippocampus and triggered by connectivity with the amygdala, such as the instance of PTSD (Stahl, 2021). The processing of these fear responses is regulated by specific neurotransmitters working with the amygdala, that include GABA, dopamine and serotonin, as well as voltage gated calcium channels.
Worry
Worry is the other core symptoms in anxiety disorders thought to be secondary to malfunction of the cortico-striato-thalomo-cortical loops (CSTC) of the prefrontal cortex, mediated by GABA, serotonin, norepinephrine, glutamate, dopamine, and voltage-gated calcium ion channels, resulting in anxious misery, catastrophic thinking, obsessions, and apprehensive expectations. These regulating neurotransmitters overlap with those known to modulate the amygdala (Stahl, 2021).
Questions
- Comorbid symptoms in major depressive disorder (MDD) and several anxiety disorders are:
- Sleep disturbances and fatigue
- Concentration
- Psychomotor arousal
- All of the above
The correct answer is all of the above (NKU, 2024). There are many overlapping qualities such as the neurotransmitters and networks involved, in addition to the noted symptoms (Stahl, 2021).
- Age of onset risk of Anxiety in children is
- 4-6 years of age
- 6-12 years of age
- 10-14 years of age
- >12 years of age
The correct answer is 6-12, as noted in lecture materials (NKU, 2024).
References
Northern Kentucky University. (2024). MSN 671 Psychopharmacology, Module 5 Lecture Material.
Stahl, S. M. (2021). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (5th ed.). Cambridge University Press.
Tzouvara, V., Kupdere, P., Wilson, K., Matthews, L., Simpson, A., & Foye, U. (2023). Adverse childhood experiences, mental health, and social functioning: A scoping review of the literature. Child abuse & neglect, 139, 106092. https://doi.org/10.1016/j.chiabu.2023.106092
Post 2
Discuss the amygdala’s role in anxiety.
There are two core symptoms of anxiety, fear and worry (Stahl et al., 2021 p. 364). Fear is controlled by the amygdala, a limbic structure that is a principal neural circuit thought to regulate anxiety (Nuss, 2015). Imaging studies on humans has shown electrical stimulation of the amygdala leads to fear and anxiety (Nuss, 2015). Additionally, functional imagery studies found the amygdala was activated in response to stimuli in patients with anxiety disorders more than non-anxious controls (Nuss, 2015).
The amygdala is divided into two structures, the basal lateral amygdala complex (BLA) and central medial amygdala complex (Nuss, 2015). Negative stimuli are received into the BLA, from the thalamus, which activates the central medial amygdala complex through the release of glutamatergic pathway while also activating inhibitory GABAergic interneurons (Nuss, 2015). This creates the affect of anxiety. Normal anxiety responses stimulate motor responses such as fight or flight, release cortisol, and increase breathing (Stahl et al., 2021 p.364 – 365).
Compare and contrast how fear and worry are thought to be regulated.
Fear and worry are the two main symptoms associated with anxiety. Fear is regulated through the amygdala, whose neurobiological regulators are GABA, serotonin, norepinephrine, and voltage calcium ion channels (Stahl et al., 2021, p. 364 – 365). Worry is regulated by the cortico-striato-thalamo-cortical circuit, whose neurobiological regulators are GABA, serotonin, dopamine, norepinephrine, glutamate, and voltage gated ion channels (Stahl et al., 2021, p.365 – 367). There is overlap in the neurotransmitters that regulate both systems. Overlap of the neurotransmitters may cause excitability or dysfunction to a stimulus. Malfunctioning of the amygdala-centered circuits can cause symptoms of anxiety and fear while malfunctioning of the cortico-striato-thalamo-cortical circuits can cause symptoms of worry, such as anxious fear, apprehensive expectations, and obsessions (Stahl et al., 2021, p364 – 367)
- What other disorder’s symptoms, circuits, and neurotransmitters overlap with anxiety disorders?
- Schizophrenia
- ADHD
- Dementia
- Major Depressive Disorder
Answer: D, major depressive disorder. Fatigue, sleep difficulties, problems concentrating, and psychomotor symptoms are common with both anxiety disorders and major depressive disorders, which can increase the risk of misdiagnosing. However, core symptoms are not the same and when assessing a patient, it is important to ensure the core symptoms associate with the diagnosis prescribed (Stahl et al., 2021 p. 360-361).
- What is the best way to identify unipolar from bipolar?
- Obtain a family and social history
- Prescribe an SSRI
- Refer to a therapist
- Prescribe lithium
Answer: A, obtain a family and social history. There is no good way to identify between unipolar and bipolar, however, a thorough clinical history can help make the diagnosis easier. Stahl et al. (2021) suggest asking two questions “ who’s your daddy?â€, meaning what is your family history, and “where’s your momma†meaning additional history will need to be obtained from someone close to the patient.
Philippe Nuss (2015) Anxiety disorders and GABA neurotransmission: a disturbance of modulation, Neuropsychiatric Disease and Treatment, , 165-175, DOI: 10.2147/ NDT.S58841
Stahl, S. M., Grady, M. M., & Muntner, N. (2021). Chemical Neurotransmission. In Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (pp. 224-282, pp. 359-378). Cambridge University Press.