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Brain and Behaviour > Emotional Brain- Depression and Antidepressants > Flashcards

Emotional Brain- Depression and Antidepressants Flashcards

1
Q

What is primary depression?

A

Depressive symptoms in isolation (depression on its own)

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2
Q

What is secondary depression?

A

Depression caused by another psychological or physiological condition. Ex: thyroid problems, demntia, etc.

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3
Q

1st demension of depression: two types?

A

SEVERITY
Mild: dysthymia
Severe: major depression

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4
Q

2nd dimension of depression?

A

CYCLICITY
unipolar: depressive episodes only
Bipolar: depressive and MANIC episodes (Sometimes rapid cycling)

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5
Q 
Other terminology for:
mild unipolar
mild bipolar
severe unipolar
severe bipolar
A

mild unipolar=dysthymia
mild bipolar=cyclothymia
severe unipolar=unipolar major depression
severe bipolar=bipolar disorder

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6
Q

How does the depressive scale go?

A

Depression-Melancholia-Normal-Hypomania-Mania

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7
Q

What was depression historically referred to as?

A

melancholia. Later= depressive personality disorder

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8
Q

What are the symptoms of major depression?

A 
Anhedonia (cannot feel pleasure in enjoyable things)
Psychomotor retardation (or agitation during manic phases, if applicable) > motor is suppressed, movement is difficult, hard time getting up -> dopamenergic system
Sleep problems (hyposomnia- sleeping less than normal) or hypersomnia
Eating problems (hypophagia=eating less than normal) or hyperphagia 
Elevated glucocorticoids (cortisol) in 50% of major depression cases
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9
Q

What symptoms are prevalent in milder depression?

A

Hypersomnia more prevalent (as in SAD)
Hyperphagia (as in SAD-carb cravings)
-other symptoms not usually part of milder depression

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10
Q 
Complete chart:
For melancholic (mild depression) and Atypical depression:
Pattern?
Diurnal variation?
Sleep?
Eating habits?
Motivation?
Other characteristics?
Prevalence?
A

Melancholic:
Phasic, Worse in the AM, Morning insomnia(early awakening), hypophagia/anorexia, ahedonia/loss of interest, psychomotor agitation and mental pain, 40-60%

Atypical: Chronic, worse in PM, hypersomnia, hyperphagia/weight gain, anxiety prominent (good response to some SSRIs and MAOIs, cheer up when good things happen, 15%

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11
Q

Neurotransmission + depression:

What happens with reuptake?

A

neurotransmitter is recycled + repackaged for future use by axon terminals

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12
Q

Degradation?

A

neurotransmitter is degraded and flushed- in cerebrospinal fluid then blood, then urine

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13
Q

What happens if the clearing of the neurotransmitter fails? (no reuptake or degradation?)

A

More NT remains in the synapse and a stronger signal is processed by the receiving neuron

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14
Q

What is monoamine theory?

A

An NE hypothesis of depression

NE- main NT involved
ex: in bipolar disorder, an actual depressive episode is depletion of NE and a manic episode is an excess of NE

serotonin (5-HT): to a lesser an extent (by the way, 5-HT is an indoleamine, as opposed to a catecholamine)

dopamine (DA): to a much lesser extent
Antidepressants supporting this theory: TCA’s, MAOI’s, heterocyclics

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15
Q

When does the monoamine theory apply best?

A

In the context of a cyclical disorder (cyclothymia or bipolar).

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16
Q

What is the serotonin theory?

A

Serotonin is the exclusive suspected neurotransmitter.

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17
Q

What are the antidepressants used in serotonin theory? Are they efficient? example of one.

A

SSRI’s

-Some very efficient: IF depression and anxiety combined (ex: Paroxetine)

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18
Q

What are the problems associated with SSRI’s (3 S’s)

A
  • suicide
  • SSRI withdrawal
  • serotonin syndrome
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19
Q

What happens if NE or 5-HT levels are decreased in normal people? Study?

A

They are likely to become depressed.

In some treatments of hypertension, an artificial decrease of NE leads to low blood pressure but CAUSES depression.

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20
Q

What is norepinephrine involved in, via its affect on the ANS?

A

The four 4’s,Fighting, fucking, fleeing, feeding.

21
Q

What is the pleasure pathway hypothesis?

A
  • from self-stimulation studies on rats
    pathway: -rich in NE and DA receptors
  • lack of NE or DA could cause anhedonia (inability to feel pleasure)
22
Q

What is the motor pathway hypothesis?

A
  • from motor pathway stim in rats/levels of activity
  • inability to do things (helpless/passive) : psychomotor retardation
  • motor functions rely on NE and DA in motor pathways
23
Q

What are problems with the NE and 5-HT hypotheses?

A

Timing: Antidepressants can change NE and 5-HT signalling within hours but takes weeks for subjects to feel better.

24
Q

What is the dysregulation hypothesis of depression?

A

-Too much or too little NE or 5-HT is the problem.

25
Q

Antidepressants: What are the factors of too much NE or 5-HT?

A

“Down-regulation” at the receiving neuron

  • How much is the emitting neuron producing?
  • How sensitive is the receiving neuron? (how many receptors?)
26
Q

Normally, If depression is caused by a surplus of NE and 5-HT, and If TCA’s or MAOI’s are prescribed…

A

The consequence will be a dramatic increase in NE and 5-HT. If it is true that there is too much NE or 5-HT to start with:

Initially, the depressive symptoms following intake of TCA’s or MAOI’s should be worse (there is evidence for this with both TCA’s and MAOI’s).
After a while, down-regulation should occur… the person will eventually (and likely) feel better.

27
Q

Antidepressants: The problem is too little NE or 5-HT?

Options?

A

The axon terminals of the sending neuron release:
autoreceptors: they will respond to
neurotransmitter molecules that “come back”. These returning neurotransmitter molecules act like a feedback signal.
This feedback is necessary for “decision making” at the pre-synaptic level.

Options:
Release more neurotransmitter? or Synthesize more neurotransmitter?

28
Q

What if the autoreceptors of the sending neuron can make wrong evaluations (likely underestimating the amount of released neurotransmitters)?

What happens when antidepressants given?

A

The autoreceptors make wrong decisions&raquo_space;> Strong down- regulation of the autoreceptors.
This down-regulation sends the message: “you’re releasing too little NE and/or 5-HT”.
Consequence: increase in the synthesizing and releasing of NE and 5-HT.
In depressive individuals we already have too little NE and/or 5- HT.

Antidepressants are given&raquo_space;> increase in the signalling of NE and 5-HT.
Consequence: increase in signalling will cause down-regulation of NE / 5-HT receptors (receiving neuron).

29
Q

KEY ISSUE of too little NE or 5-HT in antidepressants?

A

KEY ISSUE: the autoreceptors on the releasing neuron (sending, emitting) will down-regulate more than the receptors on the receiving neuron.
This will cause an even greater increase of NE / 5-HT signalling.
The individual feels better because the releasing neuron will release sufficient amounts of NE / 5-HT to overcome the lack of sensitivity of the receiving neuron.

30
Q

MAO inhibition or NE reuptake blockade can act on which receptors and autoreceptors?

A 
alpha2-autoreceptor
beta-receptor
alpha2-somatodendritic autoreceptor
alpha1-receptor
alpha2-receptor
31
Q

What is the effect of antidepressants, ECT and sleep deprivation? Result?

A

•
Reduction in autoreceptor responsiveness.
This causes a gradual increase in NE cell firing and turnover.

32
Q

PET scan studies and depressive individuals results?

A

Less active: caudate nucleus (basal ganglia) suggesting a dopamine involvement. (ability to make decisions- very indecisive)
• More active: amygdala.
This may support the “psychomotor retardation/agitation” theory.
• More active: frontal cortex; hemispheric bias?
This may support the overactive HPA/ANS/ limbic system theory

33
Q

How can thyroid hormones affect depression?

A

can ameliorate depressive symptoms, including the ones occurring during PMS
• •
TRH (thyrotropin releasing hormone; from the hypothalamus): low in depressed patients
TSH (thyroid stimulating hormone or thyrotropin; from the anterior pituitary): low in depressed patients

34
Q

How can pituitary hormones affect depression?

A

unclear, but apparent impaired responses of the following:
GH
Prolactin

35
Q

How can gonadal hormones affect depression?

A

Estrogens: low levels&raquo_space;> depression (involved in, PMS, PPD, PMD/ menopause?) or at least fluctuations with progestogens
Progestogens: see above (evidence from PMS, PPD, PMD) Androgens: low levels&raquo_space;> depression (mainly testosterone; andropause?).

36
Q

How can pineal hormone affect depression?

A

Pineal hormone: Low melatonin* production (made from serotonin)

37
Q

How can adrenal hormones affect depression?

A

Adrenal hormones: high levels in (50%) depressed humans.
•
•
DHEA: weak androgen in sharp decrease during aging. Corticosterone: high levels in rodent models of depression. Cortisol: see below.
• ! Glucocorticoids (or corticosteroids)
• •
•
Depression = overactive HPA axis? Limbic system? Autonomic nervous system?
High glucocorticoid production (adrenal glands [cortex]) because of high ACTH production (from the pituitary gland). Hypothalamic cells are over-excited by the limbic system.
Hypothalamus&raquo_space;> CRH&raquo_space;> Pituitary gland&raquo_space;> ACTH&raquo_space;> adrenal cortex&raquo_space;> cortisol

38
Q

What are cortisol levels linked to?

A

• •
•
•
Cortisol connection
linked to dysfunction in circadian rhythms? disinhibition of the HPA axis?
•
•
•
• •
investigation of the CRH-ACTH-cortisol patterns direction of causality:
depression&raquo_space;> high cortisol levels ?
high cortisol levels&raquo_space;> depression ? levels of cortisol:
very low levels&raquo_space;> depression e.g., Addison’s disease very high levels&raquo_space;> depression e.g., Cushing’s disease

39
Q

Stress response can lead to?…

  • Mobilization of energy at cost of energy storage:
  • Increased cardiovascular tone
  • Suppressed digestion
  • Suppressed growth
  • Suppressed reproduction
  • Suppressed immunity/inflammatory response
  • Analgesia
  • Neural responses
A
  • Fatigue, muscle wasting, steroid diabetes
  • Hypertension
  • Ulcers
  • Bone decalcification, dwarfism
  • Suppressed ovulation, impotency, lost libido
  • Impaired disease resistance
  • Apathy
  • Accelerated neural degeneration during aging
40
Q

What are the protective effects of anti-depressants?

A

Stress&raquo_space;> high gluc.&raquo_space;> low BDNF (brain-
derived neurotrophic factors)&raquo_space;> atrophy or death of neurons (apoptosis; high in the hippocampus).

Antidepressants&raquo_space;> increase 5-HT and NE&raquo_space;> increase BDNF&raquo_space;> decrease gluc.&raquo_space;> increases survival and growth of neurons.

41
Q

Animal models of depression-problems?

A

There are no animal models of depression that mimic all the symptoms of depression.
All current models are models of reactive depression. They typically focus on one or a few of the following
aspects of depression:

Reduction in psychomotor activity Anhedonia
Neuroendocrine responses
Cognitive changes
Eating dysfunctions
Sleeping dysfunctions
-animals tend to live in moment, planning and existentialism not very present (due to smaller frontal lobes)

42
Q

What is reactive depression?

A

Triggered by stress (broadly defined: social or physical): Tends to involve by default the HPA axis.
(depression naturally not involving HPA axis)

43
Q

Explain depressed individuals with enlarged pituitary and adrenal glands.

A

Many depressed individuals have higher levels of cortisol, produce more cortisol than non- depressed for the same increase in ACTH.

when stressed, adrenal glands are getting enlarged
extreme stress can cause adrenal tumours
-adrenal tumours can also cause stress because of elevated levels
-stress= problem for people with diabetes, dysregulates system and insulin control

44
Q

Cortisol and depression?

A

Negative feedback loop:

when depression occurs= system unable to slow down, and stop producing cortisol, getting out of hand

45
Q

What NT’s/hormones does stress affect?

A

NE, Acetylcholine, GABA

-they regulate CortisolRH from hypothalamic cells

46
Q

What kind of levels of CRF do depressed individuals have compared with non depressed?

A

Higher CRF in their CSF and more CRF producing cells in the hypothalamus.

47
Q

What reduces CRF levels?

A

Antidepressants and ECT

48
Q

What is Dexamethasone?

A

Synthetic glucocorticoid

49
Q

What is the challenge in Dexamethasone?

Who is more likely to relapse in depression?

A

It should induce a strong downregulation of CRF and ACTH (negative feedback loop)
-this does not occur in depressed individuals)
Non-responders to DEX treated successfully with anti-depressants are more likely to relapse than those that respond to DEX.

Brain and Behaviour (4 decks)

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