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PSYT 500 > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

what is the top cause of DALY in Canada for both sexes for all ages?

A

ischaemic heart disease

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2
Q

what is the top cause of DALY in Canada for both sexes aged 20-24 yo?

A

mental disorders (drug use and depression are top)

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3
Q

how did covid-19 impact mental health?

A

prevalence increased (affected women more than men)

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4
Q

until the first half of the 20th CEN, explanation for mental illnesses was dominated by _____

A

psychoanalytic theories of Freud and colleagues

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5
Q

who advocated somatic bases of mental illnesses?

A

Kraepelin

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6
Q

(freud/Kraepelin)

______: focused on neuroses and the psychological

____: focused on psychoses and the somatic

A

freud: focused on neuroses and the psychological

kraepelin: focused on psychoses and the somatic

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7
Q

what was discovered in the 1950s that suggested the biological/brain basis of mental disorders? (2)

A

discovery of drugs effective against mental disorders

E.g., discovery of the minor tranquilizer chlorpromazine as an antipsychotic, and the demonstration of lithium as an effective anti-mania drug.

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8
Q

what transformed the field of mental disorders in the last 20-30 years?

A

Advances in neuroimaging,
neuroengineering, neurochemistry, genetics, cognitive science and electrophysiology

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9
Q

explain the following statement: “mental illnesses are diseases of the brain”

A

All mental processes are the result of genes and their protein products determining the pattern of interconnections between neurons in the brain

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10
Q

(Kandel/Wagner-Jauregg/ Moniz)

______(Nobel, 2000) is one of the three psychiatrists to have won Nobel prizes.

Other two are:________
in 1927 for malaria inoculation in the treatment of dementia paralytica, and ______ in 1949 for leucotomy in certain psychoses.

A

kandel; wagner-jauregg; moniz

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11
Q

fill in the blank of the DSM5’s definition of mental illness:

“Clinically significant behavioral or psychological ____ or pattern that occurs in an individual and that is associated with present ____ (e.g., painful symptom) and/or ____”.

A

syndrome; distress; disability

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12
Q

why is the DSM a categorical classification? (2)

A

divides mental disorders into types based on criteria sets with defining features

Each category is not a completely discrete entity with absolute boundaries.

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13
Q

DSM is ______ with regard tocauses of mental disorders.

A

atheoretical

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14
Q

why is the following statement appropriate: “The DSM has little to do with biological causes. Instead, it focuses on symptoms.” (2)

A

The specific diagnostic criteria are meant to serve as guidelines to be informed by clinical judgment

The use of criteria is meant to facilitate agreement among clinicians and investigators and ensures that clinicians use the same terms in the same ways.

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15
Q

explain the following statement: “The strength of DSM is “reliability”; however, its big weakness is lack of validity.” (2)

A

Because of paucity of information on the underlying causes of most mental disorders, DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure.

Of note, recent large scale genetic studies do not support the discreet classification scheme of DSM.

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16
Q

what is the National Institutes of Mental Health’s Research Domain Criteria (RDoC)?

A

To transform diagnosis by incorporating genetics, imaging, cognitive science, and other levels of information to lay the foundation for a new classification system.

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17
Q

In the RDoC, ___ represent the fundamental unit of analysis. Related constructs are grouped into major ____ of functioning.

A

constructs; domains

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18
Q

what are the five domains of the RDoC and where would attention/memory and fear/anxiety be placed?

A

Negative Valence Systems (i.e., systems for aversive motivation) (FEAR/ANXIETY)

Positive Valence Systems,

Cognitive Systems, (ATTENTION/MEMORY)

Systems for Social Processes,

Arousal/Regulatory Systems

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19
Q

why wasnt glutamate considered to be a neurotransmitter for a long time?

A

knew it in biochem, but assumed that such a common chemical cant be a nt in the brain

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20
Q

what are the 5 characteristics mentioned in class on glutamate?

A

Non-essential amino acid

Most commonly used excitatory neurotransmitter in the brain

90% of neurons use glutamate as their neurotransmitter

80-90% of synapses are glutamatergic

Free glutamate can be found in food

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21
Q

what amino acid can also activated GluRs?

A

aspartane

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22
Q

what are the two categories of GluRs and what are in each subtype?

A

iGluR (ionotropic): NMDA, AMPA, Kainate

mGluR (metabotropic): Gr1, gr2, gr3

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23
Q

what are the receptors in each subgroup?

NMDA:
AMPA:
Kainate:
Group1:
Group2:
Group3:

A

NMDA: GluN1, GluN2 (a,b,c,d), GluN3 (a,b)
AMPA: GluR1-4
Kainate: GluK1-5
Group1: mGluR1, mGluR5
Group2: mGluR2-3
Group3: mGluR4, mGluR6-8

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24
Q

what are the differences and similarities among AMPA and NMDA receptors?

A

both let Na+ in and let K+ out

NMDAR needs glutamate and excitation (to remove Mg+ ion)

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25
Q

how does NMDAR hypo function relate to schizophrenia? (3)

A

NMDA receptor antagonist-induced psychosis (ie hallucinations, out of body experiences)

NMDA receptor antagonist impairs working memory

Decrease in NMDA receptor expression (schizophrenia associated with decreased NMDAR expression)

26
Q

how do NMDAR relate to depression

A

Ketamine (NMDAR antagonist) acts as an antidepressant (decrease in depression score vs control)

27
Q

why is Ketamine such a “good” antidepressant? (2)

A
  1. effect of ketamine is very fast
    - usual antideps (like ssri) take weeks vs ketamine that takes a few hours
  2. patients are resistant to ssri (dont respond to traditional means of tx dep but respond rly well to ketamine)
28
Q

what’s a disadvantage of using ketamine to treat depression?

A

dangerous side effects

29
Q

what are the differences in synaptic vs. extra synaptic NMDARs and how do they relate to depression?

A

stimulation of synaptic NMDARs, leads to the build-up of a neuroprotective ‘shield’, whereas stimulation of extrasynaptic NMDARs promotes cell death

ketamine blocks synaptic NMDARs – overactivation of NMDARs located outside of the synapse plays a major role in NMDAR toxicity, whereas physiological activation of those inside the synapse can contribute to cell survival, raising the possibility of therapeutic intervention based on NMDAR subcellular localization

30
Q

(norepinephrine/epinephrine)

____: cause arousal and alertness

____: involved in the regulation of memory formation by emotion

A

NE/epinephrine; NE

31
Q

what is the locus coeruleus responsible for?

A

sending NE for output to forebrain and other regions

32
Q

what are the steps to creating norepinephrine?

A
  1. L-tyrosine uses tyrosine hydroxylase to become L-Dopa
  2. L-Dopa uses L-amino acid decarboxylase to become dopamine
  3. using vesicular monoamine transporter and dopamine beta hydroxylase to become NE
33
Q

what are the two types of NE receptors?

A

alpha (on pre and post synapse) and beta (only on post synapse)

34
Q

(T/F): antidepressants affect NE

A

true

35
Q

how does beta-adrenergic activation (NE) relate to memory for emotional events? (2)

A

when u ask people to read stories (one neutral vs arousal)

aroused stories (emotionally triggering events) are more easily remembered/memorized
- this affect is gone if people are treated with propronol (beta-adrenergic blocker)

36
Q

how do the LC, NE and amygdala relate? (3)

A

important brain regions for role of ne in the formation of memories of emotional events

  1. lc activated
  2. ne released
  3. activates amyg (fear)
    3.1. central amyg releases hormones that activates lc further (CRH)

after stress, comes with sx to shut down this alert state –> opioids can reduce activity of LC

37
Q

summarize the changes in hormone secretory patterns in response to a stressor seen in class (3)

A

activity of catecholamine release is very fast, but release of glucocorticoids takes minutes

biological effects: since catecholamines are very fast, affects memory formation and cardiovascular system

glucocorticoids requires gene expression (explains delay), also comes out of adrenal glands (must travel to brain, takes time)

38
Q

what causes the following:
1. generates heightened excitability or arousal
2. induce perceived aversiveness
3. produce lack of controllability

A

stress

39
Q

what is the most important pathway for stress?

A

HPA axis

  1. hypothalamus secretes CRH to pituitary
  2. pituitary releases ACTH to adrenal gland
  3. adrenal gland releases glucocorticoids (cortisol)
40
Q

how does stress induce perceived aversiveness ?

A

The increased cortisol levels and altered activity in emotional centers can contribute to the perception of aversiveness or negative emotions associated with the stressful situation.

41
Q

how does stress produce lack of controllability?

A

group that cannot escape shocks will lose the intention to escape (learned helplessness)

these groups show more symptoms related to mood disorders (since lack of controllability makes them think theyll be in aversive state for longer)
—-makes event seem more stressful

42
Q

what are the receptors for cortisol? how are they different?

A

Mineralocorticoid receptors and glucocorticoid receptors

the mineralocorticoid receptors require a TF

43
Q

(Mineralocorticoid/glucocorticoid)

____: (type I high affinity Cort receptor) are activated by basal level of Cort – important for mediating the effects of stress

____: (type II low affinity Cort receptor) are activated by stress level of Cort

A

Mineralocorticoid; glucocorticoid

44
Q

explain allostatic load (3)

A

needs to be shut down by cortisol (released to make system go back to normal)

if stress experience is long term, start to have high levels of cortisol which can cause changes to brain (in short term –> good adaption // long term –> triggers allostatic load (biological changes))
—pathological in long term

allostatic load –> makes brain susceptible to disorders related to stress (like depression)

45
Q

what four characteristics of DA were covered in class?

A

related to reward and pleasure (motivational control and drug addiction)

first discovered by carlsson in 1957

also important for motor control (ie PD) – death of da neurons

haloperidol used to treat schizo (antipsychotic drugs block D2R)

46
Q

what is the mesolimbocortical pathway?

A

transports dopamine from the VTA to the nucleus accumbens, amygdala, and hippocampus.

The nucleus accumbens is found in the ventral medial portion of the striatum and is believed to play a role in reward, desire, and the placebo effect.

47
Q

what are the steps to the synthesis of DA?

A
  1. L-tyrosine uses tyrosine hydroxylase to become L-Dopa
  2. L-Dopa uses L-amino acid decarboxylase to become dopamine
48
Q

how do cocaine and amphetamine affect DAT (DA transporter)?

A

Cocaine is a nonselective competitive inhibitor of all monoamine transporters (increase [DA] in synapse

Amphetamine and related drugs are substrates of these transporters. These drugs cause redistribution of the monoamines to the cytoplasm and their release through DAT (more [DA] in cytoplasm (extracellular space))

49
Q

what three characteristics of serotonin were discussed in class?

A

Implicated in wide range of functions: cardiovascular and respiratory activity, sleep, aggression and sexual behavior, nutrient intake, anxiety, mood, motor output, neuroendocrine secretion, and nociception and analgesia

drugs that inhibit transporter of 5-HT are potent antidepressants

activation of some 5-HT receptors is related to the hallucination effect of LSD

50
Q

where does the name “serotonin” come from?

A

The name “serotonin” reflects its early association with blood serum and its identification as a substance derived from tryptophan.

51
Q

what is the raphe nucleus?

A

can be divided into the rostral and caudal raphe nuclei, which project to the brain and the spinal cord, respectively

52
Q

what can the rostral raphe be divided into?

A

dorsal and median raphe nuclei

53
Q

(dorsal/median raphe nuclei)

___: axons are fine and rarely make synaptic contacts (more common)

___: axons are coarse and show synaptic specializations

A

dorsal; median

54
Q

how is serotonin generated?

A
  1. l-tryptophan uses TrH to become 5-HTP
  2. 5-HTP uses AADC to become 5-HT
55
Q

how do we get tryptophan?

A

we canot synthesize tryptophan ourselves –> get it from food diet (ie turkey)
– bc of this, we can control it by changing diet (if we want to modulate 5ht)

56
Q

what happens if you give L-DOPA to the 5HT terminal?

A

generates serotonin and dopamine (since uses same enzymes)

57
Q

how many types of 5HT are there total and how many are in the brain/pns?

A

7 total; 7 in brain; 2 in pns

58
Q

what three characteristics about SERT (serotonin transporter) were covered in class?

A

Encoded by SLC6A4 on chromosome 17q

Two polymorphic forms of SLC6A4 promoter: a long form that contains 16 repeats of a GC-rich, 20—23-bp-long elements, and a short form that contains 14 repeats. The short form increases risk of depression

Chronic exposure to SERT inhibitors (SSRI) decreases 5-HT uptake, perhaps by inducing internalization and degradation of the transporter proteins

59
Q

what happens if there is too much 5HT ?

A

too much 5ht in body can cause diff symptoms

(increase in blood presure and body temp) – can be lethal

affects people who take 5ht targeting drugs (that increases 5ht in brain)

60
Q

explain the non-vesicular release of 5HT caused by ecstasy (2)

A

Synaptically released 5-HT are reuptake by specific transporter SERT

Ecstasy blocks VMAT raises the level of 5-HT in the cytoplasm. The increase in cytoplasmic 5-HT reverse the direction of presynaptic transporter, which results in nonexocytoticrelease of 5-HT

61
Q

what is magnetic resonance spectroscopy?

A

used to study diff effects of nt and see their roles
- measure level of nt (ie glu or gaba) in particular brain regions by studying spectral changes
—higher resolutions are more accurate
- can study changes in levels of the nt during wake, sleep, tasks, etc

PET ligands –> see changes in levels of other nt

62
Q
A

PSYT 500 (11 decks)

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