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PMCOL 412 > Mood Disorders II > Flashcards

Mood Disorders II Flashcards

1
Q

SSRI goal

A

to work on 5HT and NA
Without affecting Histamine, Muscarinic ach receptors or adrenergic receptors
i.e. have the same mechanism as TCAs w/o TCA side effects

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2
Q

How SSRIs work

A

prevent reuptake of 5HT by SERT –> increase 5HT in synapse

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3
Q

5HT precursor is

A

tryptophan

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4
Q

Best known SSRI

A

fluoxetine

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5
Q

Fluoxetine uses

A

Best known SSRI

Used for MDD, OCD, bullemia nervosa, panic disorder and premenstrual dysphoric disorder

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6
Q

SSRI uses

A

Most used ADs but also used for anxiety

and OCD, bullemia nervosa, panic disorder and premenstrual dysphoric disorder

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7
Q

SSRI side effects

A
  • Anorexia, insomnia and drug interaction
  • Can cause serotonin syndromes –> tremor, hyperthermia and cardiovascular collapse
  • Lower affinity for mAchRs therefore fewer anti-cholinergic effects
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8
Q

NRIs (noradrenaline uptake inhibitor)

A
  • NA specific

- Block activity of NET –> Accumulation of NE in synaptic space

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9
Q

Pathway for NE formation

A

Tyrosine –Via TH –> DOPA –> dopamine –> NE

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10
Q

NRI examples

A

Atomoxetine–ADHD in children
Reboxetine–most specific; Used for MDD and off label use for panic disorder and ADHD
Viloxazine–AD; Stimulant like amphetamine w/o dependence

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11
Q

Atomoxetine

A

NRI used for ADHD in children

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12
Q

Reboxetine

A
  • most specific NRI
  • Used for MDD
  • Also used off label for panic disorder and ADHD
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13
Q

Viloxazine

A

NRI used as AD

Stimulant like amphetamine w/o dependence

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14
Q

NRI side effects

A

Hypertension, increased HR, tremor, decreased appetite

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15
Q

NRI eliminated by

A

CYP450 in liver

therefore there is potential for interaction with drugs that induce/decrease CYP450 levels

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16
Q

SNRI (Selective serotonin-noradrenaline uptake inhibitor) examples

A

two examples: Duloexetine and venlafaxine

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17
Q

SNRI side effects

A
  • Headache, nausea, hypertension

- Also eliminated by CYP450 and can have drug interaction through CYP

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18
Q

SNRI eliminated by

A

CYP 450, can therefore have drug interactions

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19
Q

SNRI uses

A

as AD

but also effectie for anxiety and neuropathic pain

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20
Q

Duloxetine

A

SNRI used for MDD, generalized anxiety, fibromyalgia, neuropathic pain

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21
Q

Venlafaxine

A

SNRI used for MDD, generalized anxiety, panic disorder and social phobia

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22
Q

2 main ways to study mood disorders

A

In humans or animal models

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23
Q

Human research of mood disorders

A

Human research–usually observational using imaging (during tasks, or between controls and depressed patients)

Look at genes responsible–twins or GWAS

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24
Q

Imaging techniques used in human research of mood disorders

A

Imaging:
• Positron-emission tomography (PET)
• Magnetic resonance imaging (MRI)
• Functional magnetic resonance imaging or functional MRI (fMRI)

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25
Q

Genetic study of mood disorders in humans through

A

Twin studies OR Genome-wide association study (GWAS)

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26
Q

Human imaging in depression: how we study it

A

Brain scan while preforming 2 different tasks
1) Emotional discrimination task (EDT)
2) Object discrimination task (ODT)
Use FMRI to look at default mode network
Using EDT: ODT ratio–can measure whether Default mode network is activated or not

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27
Q

Depression test–how we measure depressive mood in humans

A

hamiliton depression rating scale

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28
Q

Default mode network

A

Most commonly active when brain is at active rest (ex. Daydreaming, mind wandering) or when indv is thinking of others, about the past or toward the future

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29
Q

Default mode network correlates to other networks like ______

A

Correlated with other networks

ex. Attn networks

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30
Q

EDT: OCT ratio

A

Using ration between EDT or ODT–can measure whether Default mode network is activated or not
Positive value = activated
Negative = deactivated

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31
Q

Studying default modenetwork: when goiven AD

A 
Given Escitalopram (AD) and told to come back after 2 weeks
- Measure Difference b/t first and second test (w/o AD and post-AD)
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32
Q

After given AD axis change in default mode network activation

A

X-axis changes in depression after 2 weeks

Y-axis activation of Default mode network

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33
Q

3 categories of people in depression test of default mode network

A

Non-responder = inactivation of default mode responded better
Early improver
responder

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34
Q

Non-responder =

A

inactivation of default mode; responded better

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35
Q

Why look at categories of people and default mode activation state

A

Might be able to predict whether a medication will be helpful or not based on a brain scan

36
Q

Ways to model mood disorders in rodents (tests)

A
  • Forced swim test
  • Tail suspension test
  • Learned helplessness
  • Social defeat stress
37
Q

Social defeat test

A
  • Put small mouse together with a bigger, more aggressive mouse
  • The bigger one will engage it and defeat it in every session, after ten sessions put them together but separated by a window
  • Final test: big mouse in its own area and the small mouse is left to roam
  • The amount of approaches to the large mouse indicates depression
38
Q

How approach determines depression in social defeat test

A

The amount of approaches to the large mouse indicates depression

  • Does not approach = more depression
  • More it approaches = less depressed
39
Q

Ketamine

A

A dissociative anesthetic (like PCP and DXM)
- first synthesized in 1962
- Used as anesthetic, but lacks deep
sedative effect

40
Q

Ketamine tolerance

A

Tolerance can be developed after

repeated use

41
Q

Ketamine as a AD

A

1 admin of ketamine can maybe be used for treatment-resistant depression
Goal of this study to find a drug that has the beneficial effects of ketamine w/o the side effects
First:
Compared ketamine to desipramine –> in forced swim test
Desipramine vs saline –> less time immobile with DA
Ketamine also decreased immobility in forced swim test

Ketamine is also an NMDA antagonist and they compared it to another NMDA-antag (MK 801)
Both MK-801 and ketamine reduced immobility time in forced swim test
But only ketamine was able to maintain its effect for 24 hours
Means that the AD effect of ketamine does not depend on NMDA-antagonism

42
Q

Rodent study of ketamine in depression WHY

A

Goal of this study to find a drug that has the beneficial effects of ketamine w/o the side effects

43
Q

Rodent study of ketamine in depression HOW

A

First: Compared ketamine to desipramine –> in forced swim test

  • Desipramine vs saline –> less time immobile with DA
  • Ketamine also decreased immobility

Ketamine is also an NMDA antagonist and they compared tit to another NMDA-antag (MK 801)
Both MK-801 and ketamine reduced immobility time in forced swim test
But only ketamine was able to maintain its effect for 24 hours
Means that the AD effect of ketamine does not depend on NMDA-antagonism

44
Q

Forced swim test

A

The more the mouse stays afloat without moving the more depressed

45
Q

Ketamine is an ____ _____ (antag/agonist)

A

Ketamine is also an NMDA antagonist and can be compared to another NMDA-antag (MK 801)

46
Q

Ketamine in forced swim test

A

study compared ketamine and MK-801 because of NMDA antag properties

  • Both MK-801 and ketamine reduced immobility time in forced swim test
  • But only ketamine was able to maintain its effect for 24 hours
47
Q

Does ketamine’s AD effect depend on NMDA actions

A

NO, as MK-801 another NMDA antag was not effective for 24 hours but ketamine was–citing different actions

48
Q

Ketamine metabolism

A

Ketamine can be methylated to form nor-ketamine

OR hydroxylated to form hydroxy-ketamine or hydroxy-norketamine

49
Q

Ketamine enantiomer in forced swim test

A

Hydroxynorketamine enantiomer had a simialr effect in reducing immobility in forced swim test to ketamine
2R,6R enantiomer worked BUT 25,26 enantiomer did not

50
Q

Ketamine enantiomer in learned helplessness task

A

in learned helplessness test–2R, 6R enantiomer worked at reducing depressive phenotype like ketamine

51
Q

Ketamine enatiomer in chronic social defeat test

A

Chronic social defeat stress test–2R, 6R ketamine showed more approaches to larger animal and therefore a decreased depressive phenotype

52
Q

____ enatiomer of HNK (hydroxynorketamine) ____ side effects of ketamine like ______

A

2R, 6R-HNK lacks side effects of ketamine like locomotion

Ketamine side effects in mice: Increased locomotion
2s, 6s –> increased locomotion
2R, 6R –> no increase in locomotion

53
Q

Rotarod in HNK enatiomers vs ketamine

A

Ketamine–fall immediately after 5 minutes, only acts normally after 15 mins
BUT enantiomers don’t show this initial lack of coordination

54
Q

Rotarod

A

walking on rotating cylinder–measure amount of time on the rotarod without falling
More time on it = better the motor behaviour

55
Q

Self-admin of ketamine vs. enatiomers

A
  • Animals treated with ketamine–will increase their consumption of the drug
  • While those taking 2R, 6R will not
  • Suggest 2R,6R hydroxynorketamine may be a ketamine alternative for depression treatment that lacks the side effects of ketamine (including tolerance and addiction)
56
Q

Fear

A

a complex physiological, behavioral, cognitive, and subjective response
to a threatening stimulus
• adaptive response to real threats, usually transient

57
Q

Anxiety

A

Anxiety is a longer-lasting response to danger signals that can arise from:
A. immediate circumstances (well defined danger)
B. vague indications of ill-defined events that are thought to have adverse
consequences

58
Q

Aspects of anxiety that are beneficial

A

arousal, vigilance, and physical preparedness increase the likelihood of
survival in dangerous situations

59
Q

___ in fear systems leads to anxiety

A

issues/dysregualtion

60
Q

Anxiety differs from fear due to

A

the vagueness of threat AND duration of response

If it was to a real threat and shorter term it would be helpful and adaptive (i.e. FEAR)

61
Q

Threat detection network

A

Brain regions for fear: threat detection network

Amygdala, ACC, ventromedial PFC, hippocampus, insular cortex

62
Q

Amygdala

A
  • Amygdala is the key region in threat detection network

- Regulates fear and anxiety through bidirectional connections to the ACC and vmPFC, hippocampus

63
Q

In anxiety (esp. ______) get ______ (hypo/hyperactivity) of ______ and _____ (increased/decreased) activity of ______

A

In anxiety ( esp. PTSD) get hyperactivity of amygdala and diminished vmPFC activity

64
Q

PTSD effects in threat detection network

A

Functional connectivity b/t amygdala, hipp, vmPFC, dACC and the anterior insula is deficient in PTSD

65
Q

Social anxiety and threat detection network

A

treatment with CBT has been shown to rectify the disturbances in the threat network

66
Q

4 step model of threat detection network

A

1) External events detected
a. Regions: thalamus, sensory cortex
2) External stimuli interpreted as threatening or non-threatening
a. In amygdala or hipp
3) Evaluation of stimuli
a. By VTA, NAc and PFC
4) Initiation of response

67
Q

Whether an event is interpreted as threatening or non-threatening is due to the _____________________

A

the balance b/t opposing circuits

68
Q

The balance between threat/non-threat is ____ in anxiety

A

shifted towards threat in anxiety

69
Q

Many of the ____ in anxiety are also involved in ________

A

Nuclei; depresseion

Many of the nuclei involved in anxiety are the same as those involved in depression

70
Q

Differences b/t anxiety and depression circuits

A

Main differences: NTs
Anxiety: gaba and glut
Depression: catecholamines

71
Q

Anxiety disorders characterized by

A

Excessive and enduring fear, anxiety and/or the avoidance of perceived threats
external (social situations)
internal (bodily sensations)

72
Q

Panic attack

A

abrupt fear response

73
Q

Anxiety disorders onset

A

May occur throughout life but some have a specific age of onset
Ex. Separation anxiety –mainly during childhood
Social anxiety–in adolescence or early adulthood
Panic disorders/panic disorder and GAD–age of onset varies but typically around early adulthood

74
Q

Separation anxiety onset

A

Mainly in childhood

75
Q

Social anxiety onset

A

in adolescence and early adulthood

76
Q

Panic disorders onset

A

Typically around early adulthood BUT varies

77
Q

GAD onset

A

Typically around early adulthood BUT varies

78
Q

Anxiety tretaments

A

CBT or pharmacological tretament

79
Q

Anti-anxiety drugs

A

most commonly SSRIs or SNRIs

Can also use benzos

80
Q

Benzodiazepines–alternatives for anxiety

A

Anti-epileptic drugs
(GABA - gabapentin, pregabalin)
Atypical antipsychotics (risperidone,
quetiapine)

81
Q

Benzos how they work

A

Allosteric modulators of GABA-aRs

Results in anxiolytic, muscle-relaxant, anti-convulsant props

82
Q

Issues with Benzos

A

BUT possible issues of abuse or dependence

Esp. In those with past alcohol abuse or other substance abuse disorders

83
Q

Benzo uses

A

Treat insomnia, anxiety, seizures

Also can use anti-epileptics–target GABA

84
Q

Drugs used instead of Benzos

A

Ex. Gabapentin or pregabalin–used in place of Benzo when worried about abuse

Can also use atypical antipsychotics
Ex. Risperidone, quetiapine
Might also be useful; esp. As an adjacent therapy to SSRIs

85
Q

SSRIs

A

Paroxetine. sertraline, fluoxetine, venlafaxine, citalopram

86
Q

NRIs

A

Atomoxetine, viloxazine, reboxetine, maprotiline, nisoxetine, talopram

87
Q

SNRIs

A

duloxetine, velafaxine

PMCOL 412 (35 decks)

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