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Describe findings regarding ventricles, brain activity, and circadian rhythmicity in bipolar disorder.

Enlarged ventricles-Positively correlated with number of manic episodes -Clear alterations in level of brain activity between phases of bipolar disorder Circadian rhythm -Irregular sleep-wake pattern -Abnormal melatonin secretion -Advanced peak time & increased amount in manic state -Delayed peak time & decreased amount in depressive state -Clock genes -Certain mutations & polymorphisms associated with bipolar disorder

Describe, compare, and contrast lithium and carbamazepine. What are some hypotheses as to how lithium works?

Lithium •Most effective w/ mania, and then prevents following depression •No suppression of normal feelings of emotion, no intellectual impairment •Usually begin to improve w/in 1-2 weeks •Low therapeutic index which requires regular blood tests •How does it work? Not sure... •By affecting clock genes and clock proteins •By stabilizing serotonin receptors? •Preventing shifts in sensitivity •By stabilizing glutamate transmission? •By producing proteins that help prevent cell death? •4 weeks of lithium----> increased gray matter Charbamezepine •Anticonvulsant •Stabilizes the inactivated state of sodium channels---> fewer of these channels are available to open---> brain cells less excitable (less likely to fire).

Describe, compare and contrast the monoamine theory of depression with the neuroplasticity theory of depression.

Monoamine theory •Underactivity of Serotonin and Norepinephrine Synapses •Consistent with drug effects •Depression untreated with drugs may result in proliferation of monoamine receptors (up-regulation; suggests there weren't enough before). Neuroplasticity theory •Bridges the gap between drug effect at synapse and behavioral effect •Hypothesis: Depression results from a decrease of neuroplastic processes* in the amygdala, PFC, and hippocampus à neuron loss & other neural pathology •Stress and depression associated w/ disruption of neuroplastic processes •Antidepressants increase those neuroplastic processes

Define: anhedonia, reward positivity. How do these relate to depression? How could they be used as predictive measures? How do they relate to nucleus accumbens?

Reward positivity- Reward positivity is a brain response to a gain/win Decreased reward positivity= decrease in nucleus accumbens activity Anhedonia- lack of excitement even when presented with a positive stimulus or reward. This is a symptom of major depressive disorder If this decreased pleasure i caught early you can treat for depressions sooner rather than later

Describe the diathesis-stress model of psychiatric illness.

The genetic predisposition and the environment influences the stress response

bipolar11

These major depressive disorders last at least two weeks and one hypomanic episode Symptoms of mania show: Depression Tiredness Irritability Trouble concentration Changes in sleeping habits And thoughts of sucide

What brain regions are most involved in depression? For amygdala and PFC, is activity increased or decreased? What about volume? What piece of data suggests that these alterations in volume might not be the result of depression?

amygdala , PFC- decreased Volume- decreased (genetic predisposition- Diathesis)

Describe the roles of the amygdala and prefrontal cortex in the context of emotional regulation. How do they interact with each other?

•Analysis of social situations and the proper response to them involves many brain areas and is very evolved. •Amygdala receives highly processed sensory info and responds to novel and threatening stimuli. •The "proper response to them" involves ventral prefrontal cortex •vPFC inhibitory to amygdala ---> suppression of emotional responses •SO, vPFC is interface b/t regions in control of automatic emotional responses (amygdala) and regions in control of complex behaviors

social anxiety disorder

•Increased activity in amygdala when stimulated with angry, fearful or disgusted faces •Amount of activity positively correlated with severity of symptoms

GAD

•Increased amygdala activity (shown in image) •Decreased in vmPFC •PFC couldn't suppress amygdala

Dysthymia

•Stress/trauma can trigger depressive episodes, especially in those already suffering from depression'

How are stressful experiences related to depression and to PTSD? Describe the gene-environment interaction (serotonin transporter & stressful life experiences) in the likelihood of depression.

- People who do not have a history of depression but a traumatic event occurs it usually manifests as PTSD than depression. - Researchers saw that with few stressful life events - people do not really have a high risk of depressive episode and their genotype and serotonin transporter didnt really matter - People who have increased and multiple stressful life events have a higher risk of developing a depressive disorder - Their genotype also come into play; homozygous ( short gene) have the greatest risk of depression; homozygous (long gene) have low risk and heterozygous is in between.

DCS/ bezos

- is an NMDA receptor agonist, working in conjunction with CBT - Benzos target the GABA-A receptors in the amygdala. The therapeutic effect of it is seen with decreased activity in amygdala and insula. DCS is ONLY effective with some sort of therapy and can never work alone

PTSD

-Fear conditioning in amygdala -Sensitization of brainstem pathways that are part of startle response -Failure to forget -Low cortisol as risk

What gene has been linked to anxiety disorders & what is the effect on conditioned fear and brain activity?

-For anxiety disorders they found concordance of monozygotic (identical) > dizygotic ( fraternal) - For female the COMT gene may play a role in panic disorder - A particular allele is what impairs extinction of conditioned fear and memory.

What neurotransmitter systems are involved in depression? Which are the targets of antidepressant treatment* (don't forget glutamate in that list)? How do cortisol levels differ between depression and PTSD?

. serotonin* •dopamine* •norepinephrine* •cortisol •GABA •glutamate •acetylcholine Cortisol is increased in depression and decreased in PTSD Antidepressants increase those neuroplastic processes

Compare/contrast SSRIs, SNRIs, MAOIs, tricyclics, atypical antidepressants, and ketamine.

1. SSRI's: block reuptake of serotonin (Prozac, Zoloft, Paxil, Lexapro) 2. SNRIs: serotonin and norepinepherine reuptake inhibitors (Cymbalta, Effexor) 3. Tricyclics prevent reuptake of serotonin, norepinephrine -Side effects: dry mouth, drowsiness, difficulty urinating, heart irregularities -Affect other neurotransmitters as well, hence the side effects 4. MAOIs (MAO inhibitors) block breakdown of serotonin and catecholamines -Many side effects -Interactions with other meds and certain foods which can increase BP 5. Atypical antidepressants are a miscellaneous group: -Differential affects on reuptake of serotonin, dopamine and norepinephrine -Wellbutrin: blocks reuptake of dopamine & NE but not serotonin -St. John's wort is available without prescription but may or may not work •Enhances serotonin transmission (so probably shouldn't be taken with other antidepressants (serotonin syndrome)) •Effects glutamate receptors •Interacts with other drugs 6. Ketamine: - dissociative anesthetic - NMDA receptor antagonist (but seems to have antidepressant effects at lower doses) - for drug resistant depression - multiple infusions ---> quick-acting and long-lasting antidepressant - ketamine metabolites might exert slower antidepressant effects

bipolar 1

A person may have at least one manic episode, they also may or may not have major depressive episode. Mania shows: Exceptional energy Restlessness Trouble concentrating And risky behaviours