PSYC 450 > Unit 5 > Flashcards

Unit 5 Flashcards

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1
Q

synthesis of catecholemines

A

Tyrosine –enzyme (TH)–> L-DOPA –enzyme (AADC)–> Dopamine – enzyme (DBH)–> Norepinephrine –enzyme (PNMT)–> Epinephrine

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2
Q

dopaminergic system organization

A

The dopaminergic system is organized into three main ascending pathways (nigrostriatal, mesolimbic, mesocortical) originating from the substantia nigra and VTA, with additional smaller systems in the hypothalamus and sensory structures.

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3
Q

Dopaminergic system function

A

dopamine
regulates movement,
reward
motivation,
learning
cognitive functioning

dysfunction in specific pathways contributing to disorders such as Parkinson’s disease, schizophrenia, addiction, and ADHD.

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4
Q

noradrenergic system organization

A

major norepinephrine (NE) system in the brain, neurons in the locus coeruleus (LC) in the pons. It sends widespread projections upward (“ascending”) to almost the entire forebrain.

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5
Q

noradrenergic system function

A

It regulates:
- Arousal and wakefulness
- attention and working memory, prefrontal cortex
- sensory processing
- emotion, learning and memory
- stress & fight/flight response

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6
Q

three catecholamine neurotransmitters

A

dopamine DA
epinephrine
Norepinephrine NE

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7
Q

2 dopaminergic pathways

A

1) Nigrostriatal Pathway: Coordinates movement; DA loss = rigidity, tremor.

2) Mesolimbic Pathway: Reinforces pleasure, emotion, motivation.

Mesocortical Pathway: Supports higher thinking and planning.

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8
Q

Parkinson’s disease

A

Parkinson’s disease involves a massive loss of DA neurons in the substantia nigra and consequent DA denervation of the dorsal striatum. Characterized by progressive motor dysfunction, typically beginning with tremors and advancing to postural disturbances, akinesia (lack of movement), and rigidity

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9
Q

two major families of dopamine receptors

A

D1-like receptors (which include D1 and D5) increase the activity of the enzyme adenylyl cyclase, which raises levels of cAMP inside the cell and neuron more active or excited.

D2-like receptors (which include D2, D3, and D4) do the opposite — they inhibit adenylyl cyclase and lower cAMP levels, which makes the neuron less active or inhibited.

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10
Q

what do adrenergic agonists do

A

activate α- and/or β-adrenergic receptors, mimicking the actions of norepinephrine and epinephrine producing sympathetic effects like vasoconstriction, bronchodilation, increased heart rate, and reduced NE release (α2).

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11
Q

how are adrenergic drugs useful in treating medical conditions

A
  • they target α- and β-receptors to modify autonomic functions
  • because they either stimulate or block adrenergic receptor signals to treat specific medical complications
  • B1 works with the heart
  • B2 with the lungs
  • A1 primarily vasoconstriction
  • A2 inhibit NE calming system
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12
Q

What amino acid are catecholamines derived from?

A

Tyrosine

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13
Q

What enzyme converts tyrosine into L-DOPA?

A

Tyrosine hydroxylase (TH)

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14
Q

the rate-limiting enzyme in catecholamine synthesis

A

Tyrosine hydroxylase (TH)

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15
Q

What is the product of tyrosine hydroxylase acting on tyrosine?

A

L-DOPA (L-dihydroxyphenylalanine)

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16
Q

What enzyme converts L-DOPA to dopamine (DA)?

A

Aromatic L-amino acid decarboxylase (AADC) — removes a carboxyl group.

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17
Q

What enzyme converts dopamine to norepinephrine (NE)?

A

Dopamine β-hydroxylase (DBH) — adds a hydroxyl group to dopamine.

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18
Q

What enzyme converts norepinephrine to epinephrine (EPI)?

A

Phenylethanolamine N-methyltransferase (PNMT) — adds a methyl group.

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19
Q

Where does conversion from norepinephrine to epinephrine occur?

A

Mainly in the adrenal medulla and some brainstem neurons.

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20
Q

Neurons with only TH and AADC produce which neurotransmitter?

A

Dopamine (DA) → These are dopaminergic neurons.

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21
Q

Neurons with TH, AADC, and DBH produce which neurotransmitter?

A

Norepinephrine (NE) → Noradrenergic neurons.

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22
Q

Cells that contain all four enzymes (TH, AADC, DBH, PNMT) produce which neurotransmitter?

A

Epinephrine (EPI) → Mainly in adrenal medulla cells.

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23
Q

How do high levels of dopamine or norepinephrine affect TH?

A

They inhibit TH activity through negative feedback, slowing synthesis.

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24
Q

Where is catecholamine synthesis greatest in the neuron?

A

At the nerve terminal, near synaptic vesicles — for rapid refilling.

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25
release of catecholemines
Vesicular Storage VMAT2 loads DA/NE into vesicles ↓ Trigger Action potential arrives → Ca²⁺ channels open → Ca²⁺ influx ↓ Exocytosis (release) Vesicles fuse with membrane → DA/NE released into synaptic cleft ↓ Feedback Autoreceptors detect excess DA/NE → inhibit further release ↓ ↓ ↓ Ca²⁺ channel activity ↑ K⁺ channel opening ↓ Reduced vesicle fusion → Shorter action potentials → Controlled neurotransmitter output
26
what drug exerts its effect by altering catecholamine release
Amphetamines
27
inactivation of catecholemines
Autoreceptor Feedback ↑ K⁺ channels & ↓ Ca²⁺ channels → Less release ↓ Reuptake DAT / NET → Reuptake into terminal ↓ Repackaging → VMAT2 → Vesicle reuse Breakdown Metabolism → MAO / COMT → Metabolites (HVA, MHPG, VMA)
28
What transporter loads catecholamines into vesicles?
A: VMAT2 (in brain catecholamine neurons).
29
What drug irreversibly blocks VMAT1/2, causing catecholamine depletion?
Reserpine.
30
What happens when reserpine blocks VMAT2?
DA/NE are degraded → sedation/depression; reversed by L-DOPA.
31
Which drugs release catecholamines without nerve firing?
Amphetamine and methamphetamine.
32
Difference between tonic and phasic firing?
Tonic = steady low-rate (4–5 Hz); Phasic = bursts (~20 Hz) → large DA release.
33
What proteins remove catecholamines from the synapse?
DAT (Dopamine Transporter) and NET (Norepinephrine Transporter).
34
What are the two main catecholamine-degrading enzymes (break down catecholamines)?
MAO- Monoamine oxidase COMT- Catechol-O-methyltransferase
35
How can synthesis be increased clinically?
By giving precursors like L-DOPA (used for Parkinson’s disease).
36
Where are catecholamines stored before release?
In synaptic vesicles loaded by VMAT2.
37
What triggers catecholamine release?
An action potential that opens Ca²⁺ channels, causing exocytosis.
38
How do autoreceptors control catecholamine release?
By inhibiting Ca²⁺ channels and opening K⁺ channels, which reduce further vesicle fusion and neurotransmitter release.
39
What is the main mechanism for terminating catecholamine action?
Reuptake into the presynaptic terminal by transporter proteins.
40
What are the two major catecholamine transporters?
DAT (dopamine transporter) and NET (norepinephrine transporter).
41
What happens to neurotransmitters after reuptake?
Some are repackaged into vesicles; others are broken down by enzymes.
42
D1 dopamine receptor
EXCITATORY increased cAMP and increased activity and excitement
43
D2 dopamine receptor
INHIBITORY decreases cAMP and decreases activity or inhibits it
44
Where are dopaminergic neurons primarily located?
In the midbrain, mainly in the substantia nigra (A9) and ventral tegmental area (A10).
45
What is the function of the nigrostriatal pathway?
Controls voluntary movement; degeneration causes Parkinson’s disease
46
What is the function of the mesolimbic pathway?
Mediates reward, motivation, and emotion (involves nucleus accumbens).
47
What is the function of the mesocortical pathway?
Regulates cognition, working memory, and attention in the prefrontal cortex.
48
What happens when dopamine activity is low in the mesocortical pathway?
Leads to cognitive deficits seen in schizophrenia
49
What is unique about D2 receptors?
They act as autoreceptors, reducing dopamine release and neuron firing.
50
Which receptor family has higher affinity for dopamine?
D2-like receptors, meaning they activate at lower DA concentrations.
51
Which dopamine receptor family is targeted by most antipsychotic drugs?
D2 receptors — they are blocked to reduce psychotic symptoms.
52
Dopamine agonists
act like dopamine — they stimulate dopamine receptors (especially D2/D3). restless leg and parkinsons, increase dompamine movement less feeling the need for you to move. Dopamine agonists increase dopamine receptor activity, which normalizes movement control
53
Dopamine antagonists
do the opposite of agonists — they block dopamine receptors, especially D2 receptors. This means dopamine can’t activate those receptors normally. Blocking dopamine reduces dopamine signaling in the brain, especially in the limbic system and striatum. In disorders like schizophrenia, dopamine activity is often too high, leading to hallucinations, delusions, and agitation.
54
What do dopamine antagonists do?
They block dopamine receptors, reducing dopamine activity — this helps control psychotic symptoms but can cause movement side effects if dopamine is too low.
55
Why do dopamine agonists help restless legs syndrome?
Because they mimic dopamine and stimulate dopamine receptors, restoring normal dopaminergic activity and reducing the urge to move.
56
cAMP
cyclic adenosine monophosphate a signal molecule inside cells that tells the cell to turn things on or off regulates excitement and activity of cell. High cAMP = more excitatory (D1 family) Low cAMP = more inhibitory (D2 family)
57
do neurotransmitters enter the cell
Neurotransmitters do NOT enter cells. Instead, they attach to receptors on the outside, and cAMP carries the message inside.
58
what is the ascending noradrenergic pathway
The ascending noradrenergic pathway originates in the locus coeruleus in the pons and sends widespread projections throughout the forebrain, where norepinephrine regulates arousal, attention, sensory processing, emotional memory, and stress responses.
59
What areas does the LC project to?
Cortex, prefrontal cortex, limbic system, thalamus, hypothalamus, cerebellum, spinal cord.
60
what is the Locus Coeruleus (LC)
small cluster of neurons in the pons (brainstem) that produces most of the norepinephrine (NE) in the brain
61
Main functions of ascending NE?
Arousal, vigilance, attention, sensory modulation, emotional memory, stress responses.
62
Why is the pathway called “ascending”?
The LC’s axons project upward to higher brain regions (forebrain)
63
What receptor is most important for PFC working memory?
α2A-adrenergic receptors (improve working memory).
64
How is NE pathway signaling shut off?
NET reuptake → vesicle repackaging or MAO/COMT metabolism; α2 autoreceptors reduce release/firing.
65
What happens under stress/high NE pathway?
α1 activation in PFC impairs executive function (top-down control drops).
66
how does the NE pathway work step by step?
Trigger: salient stimulus, stress, or task demand → LC neurons increase firing Release: NE is released from varicosities along LC axons in targets Receptors engaged receives and processes signals Clearance: NET reuptake (back into terminals/glia) → some repackaged; some metabolized by MAO/COMT.
67
Name two key central functions of LC-NE.
Arousal/wakefulness and cognitive control (attention/working memory).
68
What are the receptors of NE pathway
a1 a2 b1 b2
69
what are the affects of alpha and beta receptors
Receptor effects (one-liners): α1 → Constrict vessels (Clamps down) α2 → Autoreceptor → Abates NE release β1 → 1 heart → ↑ rate/force β2 → 2 lungs → Bronchodilate
70
Which enzyme converts dopamine to norepinephrine?
Dopamine β-hydroxylase (DBH).
71
Where are the main noradrenergic neurons located
The locus coeruleus (LC) in the pons.
72
What does D2 autoreceptor activation do?
Inhibits dopamine release and reduces neuron firing.
73
What is the function of the nigrostriatal pathway?
Control of voluntary movement.
74
Which adrenergic receptor subtype inhibits NE release?
α2 autoreceptors.
75
What is the “fight-or-flight” response mediated by?
NE and EPI acting on α and β adrenergic receptors.
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