L15

Question 1

most common mood disorder in North America

Answer 1

Depression

Question 2

What are the symptoms of depression and what is the guideline for diagnosing depression based on these symptoms?

Answer 2

Need five out of nine in a two-week period.

ex: Psychomotor agitation or retardation

Question 3

Emotions

Answer 3

subjective feelings (anger, fear, sadness, jealousy,
embarrassment, joy) — Limbic System

Question 4

Motivation:

Answer 4

behavior that is purposeful and goal directed —

Mesocorticolimbic dopamine system

Question 5

Limbic Brain

Answer 5

a cortical border
circling the brainstem: “cerebri
limbus” (limbus=border/edge)

Question 6

Limbic Brain: An evolutionarily ‘old’ ____ that
includes the ___, ____,
__ ___ and ____ gyrus with
connections to the ___ cortex and ____.

Answer 6

An evolutionarily ‘old’ neocortex that includes the amygdala, hippocampus,
basal ganglia and cingulate gyrus with connections to the frontal cortex and hypothalamus.

Question 7

t/f: patients with major depression disorder and health controls were shown images of emotionally evocative facial expression

Answer 7

t

Question 8

Major depression disorder

Answer 8

Associated with increased engagement of Limbic regions (amygdala) and decrease engagement of regions involved in motivation (striatum) compared to healthy individuals

Question 9

changes in brain activity reflect changes in _____
release and/or _____
response

Answer 9

changes in brain activity reflect
changes in neurotransmitter
release and/or postsynaptic
response

Question 10

Neurotransmitter is concentrated within the _____ region may be involved in mediating depression

Answer 10

Limbic

Question 11

monoaminergic neurotransmitters (3)

Answer 11

Dopamine, norepinephrine, serotonin

Question 12

monoaminergic neurotransmitters do/don’t have overlapping synthesis and catabolic pathways

Answer 12

do

Question 13

monoaminergic neurotransmitters do/don’t have a “modulatory” role in the brain,
and are involved in mood, arousal, attention

Answer 13

do

Question 14

alterations in monoaminergic neurotransmitters

are associated with

Answer 14

mood disorders

among other things

Question 15

Depression results from inadequate monoamine neurotransmission (esp. ___ and ____) in the brain

why?

Answer 15

Depression results from inadequate monoamine neurotransmission (esp. serotonin and noradrenaline) in the brain

May be due to: last neurotransmitter release, fewer receptors, impaired signal transduction

Question 16

amine hypothesis:
Originated from serendipitous
observations that manipulation of the
____ system influences depression symptoms (i.e. drugs = ____ and ___)

Answer 16

Originated from serendipitous
observations that manipulation of the
monoaminergic system influences depression symptoms (i.e.: Reserpine and ipronazid)

Question 17

Rezerpine

what % of patients developed symptom

Answer 17

Antihypertensive drug that develops symptoms of depression

15%

Question 18

reserpine depletes
neurons of ____ and ____
transmitters

Answer 18

reserpine depletes
neurons of dopamine and norepinephrine
transmitters

Question 19

ipronazid

MAO inhibition leads to what

Answer 19

Anti tubercular drug that alleviates depression by inhibiting monoamine oxidase

leads to increased synaptic concentrations of monoamine neurotransmitters

Question 20

Drugs that restore monoaminergic levels are only moderately effective in __ - __ % of patients

Answer 20

30-50%

Question 21

Inconclusive evidence that ____ and ___ systems are

disrupted in depression

Answer 21

Inconclusive evidence that serotonin and noradrenergic systems are
disrupted in depression

Question 22

Antidepressants take _____ before clinical effect is seen, despite
immediate effects on synaptic neurotransmitter levels

Answer 22

several weeks

Question 23

depression associated with reduction

glutamatergic signaling in the______

Answer 23

cortex

Question 24

• loss of glutamatergic signaling impacts
both ___ and ___ function
leading to ____to noise

also impacts what (4)

Answer 24

• loss of glutamatergic signaling impacts
both excitatory and inhibitory function
leading to reduced signal to noise

long-term potentiation, neurotrophics production, synapse formation, Gene transcription (essentially brain remodeling)

Question 25

Monoamine antidepressants increase synaptic levels of monoamine neurotransmitters (particularly ____ and ____)

Answer 25

Monoamine antidepressants increase synaptic levels of monoamine neurotransmitters (particularly norepinephrine and serotonin)

Question 26

MAO

Answer 26

``` Monoamine oxidase (MAO) is an enzyme involved in breakdown of amine neurotransmitters (serotonin, noradrenaline, and dopamine) ```

Question 27

t/f: blocking amine neurotransmitter breakdown (particularly serotonin and noradrenaline) increase synaptic levels and can improve move

Answer 27

t

Question 28

example of moa inhibitor

Answer 28

ipronazid

Question 29

how to avoid tyramine cheese reaction

Answer 29

a low tyramine diet

Question 30

tyramine

Answer 30

``` a sympathomimetic monoamine (acts like noradrenaline) and is naturally found in certain foods, such as aged cheese also degraded by MAO ```

Question 31

eating a meal rich in tyramine while taking | an MAO inhibitor can lead to

Answer 31

acute hypertension reaction caused by tyramine binding to adrenergic receptors on blood vessels and in the heart

Question 32

does tyramine have psychoactive effects?

Answer 32

no, doesn't cross blood-brain barrier

Question 33

Selective reuptake inhibitors

Answer 33

Inhibit serotonin or noradrenaline transporters, which move neurotransmitter from signups to intracellular space

Question 34

blocking Transporters leads to

Answer 34

increase the extracellular concentration of neurotransmitters

Question 35

(SSRIs).

Answer 35

selective for SET are called selective serotonin reuptake inhibitors

Question 36

SNRI

Answer 36

inhibit SET & NET

Question 37

ssri eg

Answer 37

fluoxetine

Question 38

Limitations to monoamine antidepressants (3)

Answer 38

1. drugs that restore monoaminergic levels are only moderately effective in 30 to 50% of patients 2. MAOIs, SSRIs, SNRIs take several weeks before clinical Effect is seen, despite immediate effects on synaptic neurotransmitter levels 3. lead to side effects such as nausea, indigestion, dizziness, dry mouth, weight loss (since they affect serotonin and noradrenaline level throughout body)

Question 39

ketamine is a noncompetitive ____ | receptor antagonist

Answer 39

NMDA

Question 40

t/f: ketamine is dissociative anesthetic

Answer 40

t

Question 41

how is ketamine a potential anti-depressant

Answer 41

depression associated with reduction in glutamateric signaling in the cortex ketamine causes a transient burst in glutamate resulting from blockage of NMDA receptors on GABA interneurons

Question 42

effect of glutamate burst

Answer 42

synaptic | remodeling and resetting of glutamate and GABA systems

Question 43

other downstream signaling effects of ketamine

Answer 43

(BDNF release, gene | transcription) = long term effects

Question 44

Limitation of ketamine

Answer 44

narrow therapeutic index; must be administered intravenously within hospital setting

Question 45

t/f: drugs directly targeting the downstream signalling effect events associated with synaptic remodeling may be a more effective treatment for depression

Answer 45

t

Question 46

Decreased secondary messenger (_____, _____, _____) have been reported in brains of patients with major depression at autopsy

Answer 46

Inositol, cAMP, CREB

Question 47

rolipram

Answer 47

Phosphodiesterase inhibitor that increases cAMP; may be good for depression

Question 48

Depression is a _____genous disease

Answer 48

hetero

Question 49

Ketamine effectiveness = ____%, improvement after ___ day(s) SSRI effectiveness = ___% improvement after ___ weeks

Answer 49

25, 1 | 15, 8