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PSYC3030 > Catecholamines > Flashcards

Catecholamines Flashcards

1
Q

Activation of terminal autoreceptors inhibits dopamine release, in part, by

a. decreasing Na+ entry into the terminal
b. decreasing Ca2+ entry into the terminal
c. preventing reuptake into vesicles
d. increasing Cl- entry into the terminal

A

b. decreasing Ca2+ entry into the terminal

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2
Q

The A9 and A10 cell groups are also known as the ___ and the ___, respectively.

a. substantia nigra; ventral tegmental area
b. ventral tegmental area; locus coeruleus
c. substantia nigra; locus coeruleus
d. ventral tegmental area; substantia nigra

A

a. substantia nigra; ventral tegmental area

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3
Q

A scientist investigating a newly identified receptor in rat cortex determines that it is a metabotropic receptor that regulates membrane-bound K+ channels in some cells and inhibits adenylyl cyclase. Based on these findings, the receptor is most likely a(n)

a. Beta-adrenergic receptor
b. D2-like dopamine receptor
c. autoreceptor
d. D1-like dopamine receptor

A

b. D2-like dopamine receptor

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4
Q

A group of mice is given reserpine as part of an experiment. Behaviourally, these animals would be expected to show

a. increased activity
b. repetitive head and limb movements
c. stereotyped behaviours
d. sedation

A

d. sedation

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5
Q

___ and ___ exert their pharmacological effects by blocking monoamine reuptake.

a. Cocaine; reserpine
b. Reserpine; phenelzine
c. Cocaine; tricyclic antidepressants
d. Apomorphine; tricyclic antidepressants

A

c. Cocaine; tricyclic antidepressants

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6
Q

B1- and B2-adrenoceptors ___, while a2-receptors ___.

a. increase K+ channel opening; inhibit adenylyl cyclase
b. inhibit adenylyl cyclase; stimulate adenylyl cyclase
c. stimulate adenylyl cyclase; enhance free Ca2+ levels
d. stimulate adenylyl cyclase; inhibit adenylyl cyclase

A

d. stimulate adenylyl cyclase; inhibit adenylyl cyclase

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7
Q

Amphetamine and methamphetamine affect synaptic transmission by

a. shutting down the dopamine transporter and releasing dopamine back into the cytoplasm
b. releasing dopamine from vesicles into the cytoplasm and from the cytoplasm into the extracellular fluid
c. increasing catecholamine reuptake
d. increasing metabolism by MAO

A

b. releasing dopamine from vesicles into the cytoplasm and from the cytoplasm into the extracellular fluid

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8
Q

Describe the synthesis of epinephrine.

A

Tyrosine -TH-> DOPA -AADC-> Dopamine -DBH-> Norepinephrine -phenylethanolamine N-methyltransferase-> epinephrine

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9
Q

What is the name of the transporter for dopamine and norepinephrine?

A

Vesicular monoamine transporter

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10
Q

Which VMAT is located in the brain?

A

VMAT2

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11
Q

When does single-spiking mode occur for dopaminergic neurons, and what does it look like?

A

Tonic release that occurs under normal conditions (and slow wave sleep)

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12
Q

What does burst mode look like for dopaminergic neurons and when does it happen?

A

Trains of 2-20 spikes; phasic release. Occurs during REM sleep and feeding

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13
Q

What inhibits dopamine release, and how does it do this?

A

D2 autoreceptors on cell bodies, terminals, or dendrites enhance the opening of V-gated K+ channels

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14
Q

Which enzymes metabolize dopamine?

A

MAO-A (mostly in rodents) and MAO-B (mostly in humans), as well as catechol-O-methyltransferase (COMT)

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15
Q

What is the metabolite of dopamine?

A

Homovanillic acid (HVA)

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16
Q

What receptors does dopamine bind, and what kind of receptors are they?

A

D1-like (D1, D5) and D2-like (D2, D3, D4). They are metabotropic

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17
Q

Describe the mechanism of D1-like receptors.

A

Activates Gs, which stimulates adenylyl cyclase and increases cAMP

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18
Q

Describe the mechanism of D2-like receptors.

A

Activates Gi, which inhibits adenylyl cyclase and decreases cAMP production, as well as regulates K+ channels.

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19
Q

What is the nigrostriatal tract, and its function?

A

Substantia nigra (A9) to striatum. Voluntary movement (D1 is direct pathway and D2 is indirect)

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20
Q

What is the mesolimbic pathway and its function?

A

Ventral tegmental area (A10) projects to NAcc, septum, amygdala, and hippocampus. Pleasure and motivation.

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21
Q

What is the mesocortical pathway and its function?

A

Ventral tegmental area (A10) to prefrontal cortex. Cognition (attention and working memory)

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22
Q

What are en passant synapses, and in what systems are they found?

A

They are repeated swellings/varicosities along the synapse, filled with synaptic vesicles. They are found in the DA and NE systems.

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23
Q

Where does NE synthesis occur?

A

Occurs in the CNS and adrenal medulla

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24
Q

What is the mechanism that inhibits release of NE?

A

Alpha2 autoreceptors on cell bodies, terminals, or dendrites enhance the opening of V-gated K+ channels.

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25
Q

What enzymes are used to break down NE?

A

MAO-A and COMT

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26
Q

What are the metabolites of NE?

A

Methoxyhydrophenylglycol (MHPG; CNS), vanillyl-mandelic acid (VMA; PNS), and normetanephrine

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27
Q

What are the NE receptors? What type of receptors are they?

A

Alpha 1 and 2, Beta 1 and 2.

All metabotropic

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28
Q

Describe the mechanism of alpha 1 receptors.

A

Stimulate phosphoinositide second messenger system -> increase Ca2+

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29
Q

Describe the mechanism of alpha 2 receptors.

A

Reduce cAMP by inhibiting adenylyl cyclase and activating K+ channels

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30
Q

Describe the mechanism of Beta 1/2 receptors.

A

Stimulate adenylyl cyclase -> increased cAMP via Gs

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31
Q

Where is NE found?

A

CNS: cell bodies in pons and medulla of brainstem and ascending fibers to forebrain.
PNS: Sympathetic NS

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32
Q

What is the A6 group?

A

Locus coeruleus (a dense collection of NE neurons in pons) fibers extend to forebrain, cerebellum, and spinal cord

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33
Q

What are NE functions?

A

Sleep, arousal, attention, cognition (working and emotional memory via PFC by a2 receptors), and fight-or-flight response

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34
Q

What are the cognitive effects of epinephrine?

A

Memory-enhancing effect mediated by ability to increase blood glucose levels

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35
Q

What is the effect of DA transporter knockout? What disease is this a model for?

A

Lack of response to psychostimulants (e.g., amphetamines or cocaine).
Extreme hyperactivity.
Cognitive deficits and impulsivity.
ADHD.

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36
Q

What do 6-OHDA and MPTP do in mouse models, and what disease does this represent? What limitations are there to this model?

A

Damages nigrostriatal pathway.
Parkinson’s disease.
The changes are not degenerative like PD (low construct validity).

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37
Q

What is seen in mice that have a DA transporter insensitive to cocaine? What is the mechanism of this result?

A

Fail to self-administer and do not develop addiction.
In NAcc, reduced intracellular DA levels and release, reduced baseline rate of DA uptake, reduced ability of cocaine to block DAT and inhibit reuptake, reduced sensitivity of terminal D2 autoreceptors

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38
Q

What is the result of Th-knockout in mice?

A

Synthesis of all catecholamines is prevented.

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39
Q

How are dopamine-deficient mice created? What is the result?

A

Genetically knock out Th but restore gene in Dbh-expressing NE cells (to keep NE levels).
Stop gaining weight after first week and exhibit severe aphagia, adipsia, and hypoactivity.

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40
Q

How are behaviours restored in dopamine-deficient mice?

A

Injection of L-DOPA, which passes Th-mediated step and is converted to dA in dopaminergic neurons.

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41
Q

What behaviours are affected in D1 receptor knockout mice?

A

Deficits in cognitive tasks, and lack of self-administering cocaine. Reduced/no increase in locomotion after treatment with psychostimulants.

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42
Q

What behaviours are affected in D2 receptor knockout mice?

A

Impairment in spontaneous movement, coordination, and posture control. Do self-administer cocaine. Reduced/no increase in locomotion after treatment with psychostimulants.

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43
Q

What is different about D4 receptor knockout mice?

A

Hypersensitive to methamphetamine and cocaine.

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44
Q

What happens to D1 and D2 double knockouts?

A

They die in 2nd or 3rd week of life.

45
Q

How do drugs affect those models lacking NE transporters?

A

Increased sensitivity to psychostimulants

46
Q

What is PHEN, and what effect does its administration have? How does it interact with other drugs?

A

PHEN is an alpha 1 agonist.
It has increased time spent awake.
PHEN has additive effects with beta agonists.

47
Q

What is ISO, and what effect does its administration have? How does it interact with other drugs?

A

ISO is a beta agonist. It has increased time spent awake.

ISO has an additive effect with alpha 1 agonists.

48
Q

What happens when alpha 1 receptors are activated in the PFC?

A

There is a deleterious effect on cognitive functions

49
Q

What happens when alpha 2 receptors are activated in the PFC? What drugs can be used to do this?

A

Enhancement of working memory.

Clonidine and guanfacine

50
Q

What results from stress due to a one-trial passive avoidance learning paradigm?

A

Central noradrenorgic neurons increase NE release in brain.

So, NE must play a role in passive avoidance memory consolidation

51
Q

What causes Parkinson’s Disease?

A

Genetic and environmental risk factors, the biggest being age.

52
Q

What are the symptoms of Parkinson’s Disease?

A

Resting tremor, akinesia (difficulty initiating movement) and bradykinesia (general slowing of movement)

53
Q

What neurological changes occur in Parkinson’s Disease?

A

Degeneration of SNc DA cell bodies and consequent denervation of the striatum. In general, dysfunction of the nigrostriatal pathway

54
Q

What leads to the degneration of DA cell bodies in Parkinson’s Disease?

A

Mitochondrial dysfunction, oxidative stress, inflammation, excitotoxicity, protein misfolding, proteasomal dysfunction, Lewy body formation, protein accumulation, apoptosis.

55
Q

What can be used to treat Parkinson’s Disease?

A

Levodopa and Carbidopa

56
Q

What neurological difference causes ADHD?

A

Reduced DA in the prefrontal cortex

57
Q

What is schizophrenia?

A

A thought disorder characterized by illogical thinking, lack of reasoning, and inability to recognize reality

58
Q

What is the dopamine hypothesis of schizophrenia?

A

Excess DA results in positive symptoms by disruption of mesolimbic system

59
Q

What is the DA imbalance hypothesis of schizophrenia?

A

Reduced DA function in mesocortical neurons with excess DA function in mesolimbic neurons

60
Q

What is the neurodevelopmental model of schizophrenia?

A

Mesocortical cell loss occurs due to genetic or environmental events that alter brain development. They are followed by loss of inhibitory control of mesolimbic cells and onset of positive symptoms

61
Q

What are the positive symptoms of schizophrenia?

A

Delusions and hallucinations, bizarre behaviour

62
Q

What are the negative symptoms of schizophrenia?

A

Decline in normal function, reduced speech, flattened affect, loss of motivation, social withdrawal, and anhedonia

63
Q

What are the cognitive symptoms of schizophrenia?

A

Impaired working memory, executive functioning, and attention

64
Q

What can be used to treat schizophrenia, and which subset of symptoms does it treat?

A

Conventional antipsychotics that block D2 (e.g., haloperidol) help relieve positive symptoms

65
Q

How can asthma be treated?

A

Agonists that activate both alpha and beta receptors.

Most commonly, selective B2 agonist albuterol (Ventolin)

66
Q

What is levodopa, what can it be used for and what is its mechanism?

A

It is a metabolite of tyrosine and immediate precursor of DA.
It can be used to treat Parkinson’s Disease.
It increased DA synthesis.

67
Q

What side effects does levodopa have?

A

Motor fluctuations and dyskinesias

68
Q

What do amphetamines do?

A

They are sympathomimetics. They enter neurons via uptake by DAT, causing vesicles to release DA, and causing DAT to work in reverse by pumping DA into the synapse. It is an indirect agonist of catecholaminergic systems

69
Q

What are the routes of administration for amphetamines?

A

Orally, IV, or subcutaneous injection

70
Q

What disease can be treated using amphetamines?

A

ADHD

71
Q

What are the behavioural effects of amphetamines?

A

Psychosis, sensorimotor activation, increased alertness, reinforcement

72
Q

What do animal models given amphetamines do?

A

Increased locomotor activity.

At higher doses, stereotyped behaviours (repetitive movements, licking, biting)

73
Q

Does tolerance occur due to amphetamines?

A

Chronic exposure can lead to tolerance.

Few exposure can lead to sensitization and reverse tolerance.

74
Q

What is methamphetamine?

A

More potent, strong CNS effects.

Taken orally, snorted, IV, or smoked.

75
Q

How do antipsychotics function? What are side effects?

A

Reduce dopamine by being D2 antagonists.

Amotivation and anhedonia

76
Q

What are cocaine derivatives used for?

A

Procaine and lidocaine are local anesthetics

77
Q

How is cocaine consumed?

A

Converted to HCl salt and crystallized. Can be taken orally, intranasallly, IV

78
Q

What is cocaine freebase?

A

Can be smoked

79
Q

How does cocaine function?

A

They are lipophilic sympathomimetics. They block reuptake of DA, NE, and 5-HT.
At high concentrations, cocaine also inhibits V-gated Na+ channels

80
Q

What do low doses of cocaine do to animal models? High doses?

A

Low doses: increased locomotion, rearing, and mild sniffing behaviour.
High doses: focused stereotypies in a small area

81
Q

What are WIN 35,428 and RTI-55?

A

Two synthetic cocaine-like drugs that have been synthesized that are more potent, but only used experimentally

82
Q

What does alpha-methyl-para-tyrosine (AMPT) do?

A

Blocks Th, preventing overall catecholamine synthesis to counteract excess catecholamines.

83
Q

What does reserpine do?

A

Blocks VMAT to prevent DA storage into vesicles

84
Q

What happens to animal models given reserpine? How can this be treated?

A

Extreme sedation.

Sedation can be treated with DOPA.

85
Q

How do tricyclic antidepressants function?

A

Inhibits reuptake of all monoamine neurotransmitters leading to increased concentrations in the synapse

86
Q

What are the side effects of tricyclic antidepressants?

A

Histamine receptor blockade causes sedation.
Anticholinergic effects.
Alpha1 blockade leads to dangerous cardiovascular effects

87
Q

How do MAOIs work?

A

Inhibits MAO, leading to less breakdown of monoamines

88
Q

What are two examples of MAOIs?

A

Phenelzine and tranylcypromine

89
Q

How long do MAOIs take to work?

A

Biochemical changes occur within hours, but antidepressant effects require weeks of treatment.
Leads to a reduction of receptors and an up-regulation of second messengers

90
Q

What are side effects of MAOIs?

A

Inhibition of MAO in liver leads to buildup of tyramine (increased NE).
Changes in blood pressure, sleep disturbances, overeating/weight gain

91
Q

Describe an interaction of MAOIs with other drugs.

A

Drugs that enhance NE function will have a more intense effect

92
Q

What are two examples of COMT inhibitors?

A

Entacapone and tolcapone

93
Q

What can COMT inhibitors be used for?

A

Parkinson’s disease along with L-DOPA

94
Q

What does apomorphine do?

A

Stimulates D1 and D2 receptors.

Causes behavioural activation similar to that seen with stimulants

95
Q

What does SKF 38393 do?

A

Stimulates D1 receptors

96
Q

What does Quinpirole do?

A

Stimulates D2 and D3 receptors

97
Q

What does Haloperidol do?

A

Blocks D2 receptors. Lack of normal DA input causes the neurons to increase sensitivity by making more receptors.
Suppresses exploratory and locomotor behaviour. At higher doses, can result in catalepsy

98
Q

What happens to rats given haloperidol on a long-term basis?

A

Behavioural supersensitivity (receptor up-regulation)

99
Q

What does SCH23390 do?

A

Blocks D1 receptors.
Suppresses exploratory and locomotor behaviour.
At higher doses, can result in catalepsy

100
Q

What is reboxetine (Edronax)?

A

A NE transporter blocker used to treat depression

101
Q

What is atomoxetine (Strattera)?

A

A NE transporter blocker used to treat ADHD

102
Q

What is phenylephrine?

A

An alpha 1 receptor agonist used as cold medication

103
Q

What does clonidine do? What can it be used for?

A

Alpha 2 receptor agonist that inhibits SNS activity while stimulating PSNS.
Can be used for hypertension and withdrawal from opioids.

104
Q

What does dexmedetomidine (Precedex) do? What can it be used for?

A

Alpha 2 receptor agonist that inhibits SNS activity while stimulating PSNS.
Hypertension, sedation, anxiety, pain

105
Q

What does yohimbine do?

A

Alpha 2 antagonist that blocks autoreceptors and increases NE firing and release. It provokes withdrawal symptoms and drug craving in opioid-dependent patients (so is only used experimentally)

106
Q

What does prazosin do, and what can it be used to treat?

A

Alpha 1 antagonist which causes blood vessel dilation.

Can be used to treat hypertension.

107
Q

What is propranolol? What can it treat?

A 
Beta antagonist (reduces contractile force of heart).
Hypertension and generalized anxiety disorder
108
Q

What is metoprolol, and what is it used to treat? Why is it more widely used than propranolol?

A

A Beta1 antagonist that can treat hypertension.

Fewer side effects than general beta antagonist because B1 is main subtype in heart

PSYC3030 (12 decks)

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