In adults, a dysthymic mood persisting for at least 2 years punctuated by periods of major depression is commonly known as:

1. (Jessica)Compare and contrast symptoms and circuits in depression with symptoms in circuits in mania.
The symptoms of mania can consist firstly of either an irritable or expansive mood. If an expansive or elevated mood is noted, three of the following must also be present: grandiosity, increased risk-taking behavior, decreased need for sleep, distractibility, agitation or increased goal-directed behavior, loquaciousness, pressured speech, and/or flight of ideas (Stahl, 2021). If the mood is irritable, four of the above descriiptors must also be present to qualify as a manic episode (Stahl, 2021).
Clinically, a depressive episode includes either apathy or a depressed mood and must contain four or more of the following criteria: feelings of guilt and/or worthlessness, fatigue, sleep disturbances, appetite/weight changes, executive dysfunction, psychomotor agitation or retardation, and suicidal ideation (Stahl, 2021).
Theoretically, each of the symptoms for either a depressive episode, or mania, can be mapped onto specific brain circuits for which insufficient information processing may mediate these symptoms (Stahl, 2021). These regional areas of the brain in accordance with their possible symptomatology have been studied with structural neuroimaging (Jiang, 2020). Concerning depression, mental fatigue, lack of concentration, feelings of worthlessness, suicidal ideation, depressed mood, and/or reduced interest indicates an issue within the prefrontal cortex whereas the ventral striatum is the target for a lack of interest. Feelings of worthlessness, guilt, and suicidality are also linked to the amygdala (Stahl, 2021). For physical fatigue, there is an issue with the circuit that impinges on the motor striatum (Stahl, 2021). The hypothalamus is linked to insomnia and appetite changes.
In mania, motor agitation is seen in the striatum while grandiosity and racing thoughts are linked to the ventral striatum and/or the prefrontal cortex (Stahl, 2021). Mood is relegated by the amygdala and the prefrontal cortex, while arousal and decreased need for sleep is linked to the hypothalamus and basal forebrain (Stahl, 2021). The prefrontal cortex is also associated with risk-taking behavior, distractibility, pressured speech, and excessive talking (Stahl, 2021).
For both conditions, the goal is to correct the inefficient information processing in the indicated area of the brain. All these areas of the brain can be successfully innervated by either dopamine, serotonin, or norepinephrine. Prosperous targeting and treatment of neurotransmitters to specific areas of the brain can eliminate all symptoms and cause remission of a major depressive or manic episode (Stahl, 2021).
Discuss the neurotransmitters implicated in mood disorders. For this discussion, place particular emphasis on the monoamine hypothesis of depression.
The longstanding monoamine hypothesis of depression suggests that decreased monoaminergic transmission is responsible for the condition. It is theorized that the monoamine depletion causes receptors to upregulate an increasing number of receptors. It is this deficiency of one or more of these monoamines, either serotonin, dopamine, and/or norepinephrine, and too many receptors, which responds to psychopharmacological reuptake blockers. A delayed clinical effect can be seen, which corresponds with a desensitization of receptors. The delayed desensitization of receptors may be linked to neurotrophic actions through brain-derived neurotropic factor (BDNF) signaling. In essence, the sustained increased amount of monoamine causes the receptors to downregulate and reduce in quantity. It is at this time when symptoms of depression appear to improve. Regarding the brain-derived-neurotrophic factor, GABA and glutamate mechanisms may work for some patients when the monoamines do not (Stahl, 2021). Compromised neuroplasticity must be a consideration when dealing with depression as poor environmental, situational, familial, and social variables can impinge upon one’s DNA, hence rendering difficulty of BDNF expression, resulting in the compromised ability of the brain to properly make connections (Stahl, 2021). Neurotrophic dysregulation can lead to epigenetic changes, which may then cause inflammation. The inflammation leads to oxidative stress which in turn causes more hypothalamic-pituitary- adrenal dysregulation. Ultimately, this negative loop can lead to treatment-resistant depression, cognitive decline, and reduced grey matter in the brain (Stahl, 2021). Aggressive identification and treatment are the key to prevention of this cycle.
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.
1. In adults, a dysthymic mood persisting for at least 2 years punctuated by periods of major depression is commonly known as:
A.) Double depression
B.) Bipolar depression
C.) Manic depression
Answer A.) Double depression
While not listed as a diagnosis in the DSM-5, the individual components of double depression, persistent depressive disorder (PDD) and major depressive disorder (MDD) are included. The title of double depression was first mentioned following the introduction of MDD and dysthymia in the DSM-3 (Parker, 2018).
2. For some patients with depression, issues with their sleep-wakefulness cycle may hypothetically be the neurobiological basis for their condition. This phase delay is known as _______________.
A. Seasonal affective disorder
B. Circadian rhythm disorder
C. Functional circadian decline
Answer B.) Circadian rhythm disorder.
According to Stahl, for some patients, depression may be linked to a poor-functioning set of circadian rhythms (2021). The degree of circadian disorder correlates to the depression severity and can be traced to physiologically-linked measurements of elevated cortisol secretion and decreased melatonin secretion by the pineal gland (Stahl, 2021).
References
Jiang, W., Andreassen, O. A., Agartz, I., Lagerberg, T. V., Westlye, L. T., Calhoun, V. D., & Turner, J. A. (2020). Distinct structural brain circuits indicate mood and apathy profiles in bipolar disorder. NeuroImage: Clinical, 26, 101989. https://doi.org/10.1016/j.nicl.2019.101989
Parker, G., & Malhi, G. S. (2018). Persistent depression: Should such a DSM-5 diagnostic category persist? The Canadian Journal of Psychiatry, 64(3), 177–179. https://doi.org/10.1177/0706743718814429
Stahl, S. M. (2021). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (5th ed.). Cambridge University Press.
2. (Nicole) The amygdala is a structure that is located in the bilateral temporal lobes of the brain in an area called the limbic system. As we have learned before, the limbic system is important in the regulation of emotions and memories. Anxiety is a normal state of increased vigilance and responsiveness in response to a physical threat (Babaev, Chatain, & Krueger-Burg, 2018). It was once thought that the amygdala was the threat detector of the brain, or something that just triggered the fight or flight response once a person is confronted with something that is perceived as being dangerous. New studies have found the amygdala also plays a major role in establishing and evaluating positive relationships in response to our external stimuli (Sladky, Riva, Rosenberger, van Honk, & Lamm, 2021).
Pathological anxiety is thought to be caused by divergent malfunctioning of the amygdala-centered circuit and/or the cortico-striato-thalamo-cortical (CSTC) loop. The amygdala-centered circuit is responsible for the anxiety symptoms of fear, panic, and phobias (Stahl, 2021).
Studies have primarily focused on the amygdala’s ability to take sensory and cognitive information and determine whether or not there will be a fear response. When a potential fear response occurs, the amygdala-centered circuits takes over rational thought from the prefrontal cortex, it acts similar to a reflex. The external stimuli enters via the visual, auditory, olfactory, touch, and pain sensory systems, travels to the thalamus which then relays the information to the amygdala, then the information travels through the hypothalamus-pituitary-adrenal (HPA) axis, which then triggers the release of norepinephrine, epinephrine, and cortisol (Stahl, 2021). Surges of these hormones are responsible for the feelings a person has during an anxiety attack. Blood pressure, heart rate, and respiratory rate and all increased. High levels of cortisol also interfere cytokine production, which delays wound healing and the ability to fight other illnesses. Other neurotransmitters that are involved in this circuit include serotonin, GABA, and glutamate.
GABA or Y-aminobutyric acid is the principal inhibitory neurotransmitter that helps to reduce the activity of neurons in the amygdala and CSTC loops. Benzodiazepines work by enhancing GABA’s action at the amygdala and the level of the prefrontal cortex with the CSTC loop, which effectively reduces anxiety (Stahl, 2021).
The CSTC loop is similar to the amygdala-centered circuit, in that similar neurotransmitters modulate both circuits, serotonin, GABA, norepinephrine, glutamate, and voltage gated ion channels. In contrast, the CSTC loop is responsible for the anxiety symptoms of worry, anxious misery, apprehension, expectation, and obsessions (Stahl, 2021). Dopamine is an important factor in determining the prevalence of worrying. With the Met genotype, low COMT activity, and high dopamine levels, stress can decrease the ability to process information and create the symptom of worry in anxiety (Stahl, 2021).
Which neurotransmitter is specifically involved in the cortico-striato-thalamo-cortical (CSTC) loop in anxiety?
A.) Norepinephrine
B.) Serotonin
C.) Dopamine
D.) Glutamate
Answer: C.) Dopamine
Since the various genotypes for the enzyme COMT regulate the availability of dopamine in the prefrontal cortex, differences in dopamine availability may impact the risk for worry and anxiety disorders. Stahl p. 395
After a traumatic or fearful experience, stored input from the amygdala to the _______ is responsible for triggering fear when a fearful stimuli and it’s associated stimuli are encountered again in the future.
A.) Prefrontal cortex
B.) Hippocampus
C.) Thalamus
D.) Pons
Answer: B.) Hippocampus Stahl p. 409
References
Babaev, O., Chatain, C. P. & Krueger-Burg, D. (2018). Inhibition in the amygdala anxiety circuitry. Experimental and Molecular Medicine, 50 (1), 1–16. https://doi.org/10.1038/s12276-018-0063-8
Sladky, R., Riva, F., Rosenberger, L.A., van Honk, J. & Lamm, C. (2021). Basolateral and central amygdala orchestrate how we learn whom to trust. Communications Biology 4 (1), 1329. https://doi.org/10.1038/s42003-021-02815-6
Stahl, S. M. (2021). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (5th ed.). Cambridge University Press.

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