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NE Exam 2 > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What is a monoamine?

A

A class of NTs made by modifying a single amino acid

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2
Q

What are examples of monoamines?

A

Epinephrine, norepinephrine, dopamine, serotonin, histamine

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3
Q

Where do you find norepinephrine?

A

Locus ceruleus

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4
Q

What is norepinephrine associated with?

A

Wakefulness/alertness

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5
Q

Where do you find epinephrine?

A

Medulla

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6
Q

How are norepinephrine and epinephrine derived?

A

Tyrosine -> dopamine -> norepinephrine -> epinephrine

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7
Q

How are norepinephrine and epinephrine made?

A
  1. Tyrosine to dopamine via tyrosine hydroxylase
  2. Moved to vesicles where NE is created
  3. NE leaves vesicles and is converted to epi
  4. Epi moved into vesicles
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8
Q

What transporter moves epi and NE into vesicles?

A

VMAT 1 & 2

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9
Q

How are the actions of epi/NE limited?

A

Reuptake or enzymatic degradation via MAO or COMT

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10
Q

Where do you find dopamine?

A

Basal ganglia and hypothalamus/limbic system

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11
Q

What is dopamine involved in?

A

Motor control and endocrine/emotional control

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12
Q

How is dopamine made?

A

From tyrosine via tyrosine hydroxylase

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13
Q

How are dopamine’s actions limited?

A

Reuptake or catabolism by MAO and COMT

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14
Q

What does dopamine bind to?

A

Metabotropic receptors connected to G proteins.
D1 and D5 increase cAMP (in brain = neuron excitation)
D2, D3, and D4 decrease cAMP (=inhibits cell)

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15
Q

Where do you find serotonin?

A

Brainstem raphe nuclei

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16
Q

What is serotonin involved in?

A

Mood (hypothalamus/limbic system) and motor activity modification (cerebellum)

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17
Q

How is serotonin made?

A

Derived from tryptophan via tryptophan hydroxylase

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18
Q

How are serotonin’s actions limited?

A

Reuptake or catabolism by MAO and COMT

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19
Q

What does serotonin bind to?

A

5HT3 - area postrema (chemotactic trigger zone = vomiting)

5HT6 - anti-depressant effect

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20
Q

Where do you find histamine?

A

Tuberomammillary nucleus of hypothalamus

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21
Q

What is histamine involved in?

A

Wakefulness

22
Q

How is histamine made?

A

Derived from histidine via histidine decarboxylase

23
Q

How are histamine’s actions limited?

A

Reuptake or catabolism by diamine oxidase (DAO) and COMT

24
Q

What does histamine bind to?

A

H1 - PLC activation (wakefulness)
H2 - increase cAMP
H3 - decrease histamine release

25
Q

Where is Ach made?

A

Striatum of basal ganglia, midbrain, and pons

26
Q

What does Ach function in?

A

Striatum: voluntary motion

Midbrain/pons: baseline excitation to cortex and REM sleep

27
Q

What Ach receptors are in the CNS?

A

M1 (Gq increases Ca2+)
M4 (Gi decreases cAMP)
M5 (Gq increases Ca2+)

28
Q

What are the two major inhibitory amino acids in the CNS?

A

GABA and glycine

29
Q

What are GABA and glycine critical in?

A

Consciousness, motor control, vision (retina)

30
Q

How is GABA made?

A

Synthesized from glutamate via glutamate decarboxylase, transported into vesicles via VGAT, removed from synapse via GAT1 (presynaptic terminal) and GAT2 (surrounding glial cells)

31
Q

What does GABA bind to?

A

GABA A receptors that produce IPSP in adult neurons. Some are extra-synaptic receptors that function as a site of action for anesthetics
GABA B receptors: presynaptically regulate GABA release, postsynaptically inhibit postsynaptic cell

32
Q

Where is glycine found?

A

Spinal cord, medulla

33
Q

What does glycine function to do?

A

Mediates spinal inhibitions

34
Q

How is glycine removed from synapses?

A

GAT (like GABA)

35
Q

What does glycine bind to?

A

GlyR receptors, influx of chloride leads to IPSP

36
Q

Where are purines found?

A

ATP, ADP, adenosine found everywhere in CNS. Specifically in cortex, cerebellum, hippocampus, and basal ganglia

37
Q

What do purines bind to?

A

P1: presynaptic = sleep induction, inhibition of neural function. Postsynaptic = inhibition of NT release
P2: P2X and P2Y (learning/memory)

38
Q

What are some examples of peptide transmitters?

A

Opioids, tachykinins, cholecystokinin, somatostatin

39
Q

What types of opioids are there?

A

Endorphins, enkephalins, dynorphins, nociceptin

40
Q

What are the precursor molecules to opioids?

A

Proopiomelanocortinin (POMC), pro-enkephalin, pro-dynorphin, orphanin FQ

41
Q

How are opioids made?

A

Via standard protein synthesis

42
Q

How are the effects of opioids controlled?

A

Reuptake and enzymatic destruction

43
Q

What do opioids bind to?

A

Mu receptors - analgesia, respiratory depression, euphoria, constipation, sedation
Kappa receptors - analgesia, dysphoria (unpleasant)
Delta receptors - analgesia
All are metabotropic

44
Q

What are the endogenous cannabinoids?

A

Anandamide and 2AG

45
Q

Where do you find endocannabinoids?

A

Basal ganglia (mood, motor), spinal cord (modulate nociception), cortex (neuroprotection)

46
Q

How are endocannabinoids synthesized?

A

Derived from membrane lipids, synthesized in presynaptic terminal

47
Q

What do endocannabinoids bind to?

A

CB1 on presynaptic terminals in CNS

CB2 on microglia (anti-inflammatory)

48
Q

How are endocannabinoids degraded?

A

Hydrolyzed or oxidized

49
Q

What are the excitatory amino acids?

A

Glutamate and aspartate

50
Q

What do EAAs bind to?

A 
NMDA receptor (influx of calcium) with modulatory glycine binding site (required as co-agonist), modulatory magnesium binding site (blocks the channel), modulatory PCP binding site (blocks channel)
Non-NMDA receptors (AMPA and kainate)

NE Exam 2 (16 decks)

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