final

Question 1

describe the brain structure abnormalities in those with depression (4).

Answer 1

-overactive amygdala
-reduction in volume of hippocampus
-underactive and reduced dorsal/prefrontal cortex
-underactive and reduced nucleus accumbens

Question 2

how were MAOIs discovered?

Answer 2

-iproniazid was used to treat tuberculosis, and it was found that mood elevations occurred in patients
-from this discovery, the monoamine hypothesis was generated, which said that monoamine deficits cause a depressed mood
-there were issues with this theory because antidepressants increase monoamines within minutes, but symptom relief takes 2-4 weeks
-AOIs were then developed which prevent MAO from breaking down monoamine neurotransmitters

Question 3

what is the mechanism of action of tricyclics?

Answer 3

-block the reuptake of both norepinephrine and serotonin
-antagonist for cholinergic receptors which causes dry mouth, dry eyes, constipation, and urinary retention
-antagonist for norepinephrine causing negative cardiovascular effects
-antagonist for histamines causing sedative effects

Question 4

what is Ketamine? how did it come to be an antidepressant? how can it help? what are the concerns?

Answer 4

-NMDA antagonist that blocks glutamate receptors
-FDA approved nasal spray to be taken with an antidepressant; for treatment, the patient takes it twice per week then once every other week or two for maintenance
-leads to an immediate reduction in symptoms which lasts for 2 weeks
-drug abuse and acute psychedelic effects because it increases dopamine in the nucleus accumbens

Question 5

describe the response time length for antidepressants

Answer 5

-at 2 weeks, clinically significant effects occur
-full effects happen at 4 weeks

Question 6

what is the placebo effect for antidepressants? what does this imply?

Answer 6

-clinically significant improvements occur in the placebo-treated patients
-strong placebo effects and cautious clinical drug testing leads to a failure to find clinically significant effects

Question 7

what is the effect of chronic antidepressant administration on dopamine?

Answer 7

-increases dopamine in the nucleus accumbens
-increases D2 receptors in the limbic system
-increases neuronal density in limbic system

Question 8

what is an unidentified bright object?

Answer 8

part of the neurobiology of those with bipolar disorder; excessive activity in cortical white matter areas of the brain

Question 9

describe the therapeutic index of lithium

Answer 9

-narrow therapeutic index
-the gap between the effective dose and a toxic dose is small
-there is an overlap in the acute therapeutic effects and the adverse effects

Question 10

what is th mechanism of action of lithium?

Answer 10

-enters neurons through Na+ channels
-protective effects against neurodegeneration
-inhibits glycogen synthase kinase 3 (GSK-3) enzyme

Question 11

what is the current best treatment for bipolar disorder?

Answer 11

-mood stabilizers
-atypical antipsychotics + antidepressant which has a quicker response time than just antipsychotics and may have a greater reduction in symptoms than lithium
-anticonvulsants which are GABAA positive modulators, inhibit GSK-3 activity, and inhibit Na+ channel functioning which affects high-frequency action potentials

Question 12

what information does the prefrontal cortex send to the amygdala?

Answer 12

-inhibits reaction to fearful stimuli
-determines how we behave
-approach/avoid behavior

Question 13

what information does the hippocampus send to the amygdala?

Answer 13

-information about the context surrounding a stimulus

Question 14

what information does the thalamo-amygdala pathway send to the amygdala?

Answer 14

-crude, unprocessed information
-it is a short route
-does not provide fine information

Question 15

what information does the thalamo-cortical-amygdala send to the amygdala?

Answer 15

-sensory information processed in the cerebral cortex where it can be properly perceived
-it is a long route and allows for more refined information

Question 16

describe the metabolism difference between short and long acting benzodiazepines

Answer 16

-short acting benzodiazepines have a half-life of 12-24 hours
-long-acting benzodiazepines have a half-life of 20-40 hours; have active metabolites; metabolized by CYP450, CYP3A4, and CYP2C19 enzymes

Question 17

what are BZ 1 sites? where are they found? what brain areas are they found in (3) and what do they do in those areas?

Answer 17

-high affinity for GABAA receptor sites
- α1 subunit
-thalamus which causes reduced cortical arousal and reduced seizure activity
-substantia nigra which causes reduced cortical activity and reduced seizure activity
-cerebellum which causes reduced balance and coordination

Question 18

what are BZ II sites? where are they found? what parts of the brain are they found in (3) and what do they do in those areas?

Answer 18

-weaker affinity GABAA receptor sites
- α2, α3, α5 subunits
-cortex which causes reduced alertness and reduced cognitive function
-hypothalamus which causes reduced anxiety/stress response
-amygdala which causes reduced anxiety

Question 19

which antidepressants are used to treat anxiety? what is the response time? how well does it work?

Answer 19

-SSRIs and SNRIs which increase serotonin/norepinephrine
-2 weeks
-1/3 of patients are treatment resistant

Question 20

what psychological changes occur due to MDMAs empathogenic effects?

Answer 20

-may reduce resistance to thinking about an event or facilitate emotions surrounding the event
-increases the release of oxytocin
-reduces activity in the amygdala

Question 21

what is the prodromal phase? what are the signs (5)?

Answer 21

-early subtle signs of schizophrenia
signs include social withdrawal, unusual thoughts or paranoia, decreased motivation, trouble concentrating, and mild depression or anxiety

Question 22

what is a sensory gating deficit?

Answer 22

diminished capacity to filter out unimportant stimuli in one’s environment

Question 23

what are the characteristics of typical antipsychotics?

Answer 23

-D2 receptor antagonist
-reduces positive symptoms
-weak efficacy for negative symptoms and cognitive impairment

Question 24

what are the adverse effects of typical antipsychotics?

Answer 24

-extrapyramidal side effects (EPS) which include tremor, muscle rigidity, and involuntary movements due to D2 receptors antagonism in the basal ganglia
-tardive dyskinesia which is a motor disorder affecting muscles in the face and causing involuntary movements
-neuroleptic malignant syndrome (NMS) which consists of flulike symptoms, blood pressure changes, and autonomic nervous system irregularities
-hyperprolactinemia which is abnormally high blood levels of prolactin and reduced lactation, sexual dysfunction, and disruption in menstrual cycles

Question 25

what are the characteristics of atypical antipsychotics?

Answer 25

-reduce positive and negative symptoms -modest gains in cognitive functioning -reduction in depression and suicide risk -improvement in 70% of treatment resistant patients

Question 26

describe the adverse effects of atypical antipsychotics

Answer 26

-lower risk of EPS, NMS, and hyperprolactinemia -significant weight gain which can increase the risk for type II diabetes -QT interval prolongation causing prolonged heartbeat which can lead to cardiac arrest -agranulocytosis which is reduced white blood cell count in the immune system

Question 27

how do atypical antipsychotic drugs produce an effect?

Answer 27

-serotonin dopamine hypothesis states that states atypical antipsychotics are preferential antagonists of 5-HT2A compared to D2 receptors -fast D2-off hypothesis which states that antipsychotics cause rapid dissociation of drug from D2 receptors

Question 28

describe the difference between typical antipsychotics and atypical antipsychotics

Answer 28

-atypical psychotics relieve both positive and negative symptoms while typical antipsychotics help only positive symptoms -atypical antipsychotics decrease the risk of EPS, NMS, and hyperprolactinemia while these are adverse effects of typical antipsychotics

Question 29

what are the mechanism of action for atypical antipsychotics (5)?

Answer 29

-5-HT2A receptor antagonist causing weight gain -weak D2 receptor antagonist -targets the α2 adrenoceptors causing improved cognitive functioning -targets the muscarinic receptors causing dry eyes and dry mouth -targets the histamine receptors which causes sedation

Question 30

what is the DISC1 gene? what does it do?

Answer 30

-a gene that is disrupted in those with schizophrenia -the gene is important in signaling events in neurons, development of neurons, and cell migration which can cause abnormalities in cellular networks

Question 31

what is the dopamine hypothesis of schizophrenia? what is the evidence for the hypothesis?

Answer 31

-positive symptoms arise from excessive dopamine release in the limbic system causing excess in places like the nucleus accumbens -antipsychotics act as antagonists for D2 receptors and there is a correlation between D2 binding affinity and effectiveness -amphetamine and cocaine cause psychotic symptoms via increase in dopamine release

Question 32

what is the glutamate hypothesis? what is the evidence for the hypothesis?

Answer 32

-diminished levels of glutamate release throughout the cerebral cortex and limbic system -ketamine and PCP cause users to exhibit behaviors consistent with positive and negative symptoms as well as cognitive impairment -diminished glutamate may account for reduced dopamine in the prefrontal cortex and excessive dopamine in the limbic system

Question 33

which is better, the glutamate hypothesis of schizophrenia or the dopamine hypothesis?

Answer 33

-the glutamate hypothesis of schizophrenia because it accounts for both insufficient glutamate and excessive dopamine and explains all of the symptoms, not just the positive ones -low levels of glutamate in the prefrontal cortex leads to too much dopamine in the nucleus accumbens

Question 34

what are the stages of the hpa axis

Answer 34

1. alarm- increase physiological arousal in preparation for an emergency situation; hypothalamus activates sympathetic nervous system 2. resistance- sustained level of physiological arousal; hypothalamus elicits the release of ACTH from the pituitary gland; adrenal gland increases cortisol 3. exhaustion- fatigue, susceptibility to disease; immune system and metabolic activity of organs throughout the body are underactive

Question 35

what is the hpa axis? describe what happens in detail. when is cortisol released? what can prolonged cortisol increase do to the brain?

Answer 35

-hypothalamic-pituitay-adrenal axis -hypothalamus releases corticotrophin releasing factor -release of adrenocorticotropin hormone (ACTH) from pituitary gland -adrenal gland releases cortisol increases metabolism and immune system -cortisol increases during traumatic events and recall of event -prolonged increases in cortisol levels are associated with damage to the hippocampus which can cause damage to neurons, decreased volume, and memory impairment

Question 36

describe differential reinforcement of low rates test for depression. What is the effect of antidepressants?

Answer 36

-type of schedule of reinforcement where there is a period of time and if the rat presses the lever during the interval, reinforcement is pushed back and the rat has to wait another time period -antidepressants lead to more efficient responding on the task; they have a decreased response rate and an increased reinforcement rate

Question 37

describe the elevated plus maze test for anxiety. What do anxiolytics do?

Answer 37

-maze in the shape of a + elevated off the floor; two of the arms are enclosed and the other two are open; generally, rats only like to travel in enclosed spaces -anxiolytics increase time spent in open arms

Question 38

what is the diagnosis criteria for depression (2)(7)?

Answer 38

-must have either: depressed mood most of the day or markedly diminished interest or pleasure in activities -must have at least three of the following symptoms: -significant increase or decrease in appetite or weight -insomnia, disrupted sleep, or sleeping too much -lethargy or physical agitation -fatigue or loss of energy nearly everyday -worthlessness or excessive inappropriate guilt -daily problems in thinking, concentrating, making decisions -recurring thoughts of death and suicide

Question 39

what treatment would you give to someone with depression? what is the mechanism of action of the treatment?

Answer 39

-SSRIs which block the reuptake of serotonin

Question 40

what is the diagnostic criteria for bipolar disorder (1)(6)?

Answer 40

-abnormally and persistent elevated, expansive or irritable mood -at least three of the following: -exaggerated optimism -hyper sociality or sexuality -delight in everything -impulsivity and overactivity -racing thoughts; the mind won't settle down -little desire for sleep

Question 41

what treatment would you give to someone with bipolar disorder? what is the mechanism of action for the treatment?

Answer 41

-antipsychotics which are D2 antagonists -anticonvulsants which are GABAA positive modulators -mood stabilizers which enter neurons through Na+ channels and inhibit GSK-3 enzyme

Question 42

what is the diagnostic criteria for generalized anxiety disorder?

Answer 42

a person is continually tense, apprehensive, and in a state o autonomic nervous system arousal

Question 43

what is the diagnostic criteria for panic disorder?

Answer 43

-repeated and unexpected panic attacks -fear of the next attack -a change in behavior to avoid panic attacks

Question 44

what is the diagnostic criteria for a specific phobia?

Answer 44

persistent, irrational fear and avoidance of a specific subject, activity, or situation

Question 45

what is the diagnostic criteria for PTSD?

Answer 45

exposure to actual or threatened death, serious injury, or sexual violence who experience the following for at least 1 month: -re-experiencing traumatic event -avoidance of stimuli associated with the event -negative cognitions and mood including a sense of blame, detachment, anhedonia -heightened arousal including aggression, sleep disturbances, hypervigilance

Question 46

what treatment would you describe to someone with GAD? what is the mechanism of action of the treatment?

Answer 46

-buspar -5-HT1A partial agonist meaning it binds to the receptor and weakly activates it

Question 47

what treatment would you prescribe to someone with panic disorder? what is the mechanism of action of this treatment?

Answer 47

- a short-acting benzodiazepine -GABAA positive modulators meaning they increase the ability of natural GABA to bind

Question 48

what treatment would you prescribe for someone with PTSD? describe th treatment. what is the mechanism of action?

Answer 48

-MDMA assisted psychotherapy -the empathogenic effects of MDMA allow for a reduction in resistance to thinking about the event or facilitate emotions surrounding the event -increasing the release of oxytocin and reducing activity in the amygdala

Question 49

what is the diagnostic criteria for schizophrenia?

Answer 49

-disorganized and delusional thinking, disturbed perceptions and inappropriate emotions and behaviors -symptoms include: -positive symptoms: hallucinations, delusions, disorganized thoughts and speech -negative symptoms: flat effect, social withdrawal, catatonia

Question 50

what treatment would you prescribe for someone with schizophrenia? What is the mechanism of action of this treatment?

Answer 50

-atypical antipsychotics -5-HT2A receptor antagonist -weak D2 receptor antagonist targets -α2 adrenoceptors targets -muscarinic receptors targets -histamine receptor targets

Question 51

what does GSK-3 do?

Answer 51

aids in programmed cell death and regulates inflammation