Week 6 Flashcards

(61 cards)

1
Q

What is the Neuronal membrane?

A

Located on the plasma membrane of neurons, reuptake neurotransmitters from the synaptic cleft back into the presynaptic neuron to terminate signaling and recycle neurotransmitters, use Na⁺ and Cl⁻ gradients to drive the uptake of neurotransmitters against their concentration gradient, function via secondary active transport (co-transport), targets of drugs that affect neurotransmission

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2
Q

What is the Vesicular membrane?

A

found on the membranes of synaptic vesicles inside the presynaptic neuron, load neurotransmitters from the cytoplasm into synaptic vesicles for storage and subsequent release into the synapse, rely on a proton (H⁺) gradient by vesicular ATPase that pumps protons into the vesicle, an antiport mechanism drives neurotransmitter uptake,

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3
Q

What are examples of neuronal membrane transporters?

A

SERT(Serotonin), (DAT)Dopamine, (NET)Norepinephrine, (GLT-1)Glutamate, (GAT)GABA

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4
Q

What are examples of vesicular membrane transporters?

A

VMAT1/VMAT2(monoamines), VGAT(GABA/glycine), VGLUT(glutamate), VAChT(acetylcholine)

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5
Q

What is the rate-limiting step of acetylcholine (ACh) synthesis?

A
  • uptake of choline into the presynaptic neuron by choline transporter (ChT)
  • can impact both ionotropic and metabotropic receptors
  • Choline + Acetyl-CoA → Acetylcholine - done by ChAT enzyme
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6
Q

What is the function of AChE?

A

Breaks down acetylcholine into choline and acetic acid
This happens once ACh is released into the synaptic cleft, ending the signal between neurons

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7
Q

Where is AChE located?

A

Found in the synaptic cleft of neuromuscular junctions & synapses in the CNS

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8
Q

What are the catecholamine neurotransmitters?

A

Dopamine (DA), Norepinephrine (NE), Epinephrine (E),
Tyrosine hydroxylase(TH)

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9
Q

What are the steps required for Dopamine synthesis?

A

movement, reward, and reinforcement learning
synthesized when tyrosine is converted to L-DOPA by tyrosine hydroxylase, then L-DOPA is converted to dopamine by aromatic L-amino acid decarboxylase.

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10
Q

What are the steps required for Norepinephrine synthesis?

A

Sympathetic NS, attention, alertness, wakefulness
Norepinephrine is synthesized when dopamine is converted into norepinephrine by dopamine β-hydroxylase in the presence of oxygen and ascorbic acid.

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11
Q

What are the steps required for Epinephrine synthesis?

A

most of the actions are outside of the brain and used as hormones, secreted into the bloodstream, and act on peripheral tissue
Epinephrine is synthesized when norepinephrine is converted into epinephrine by PNMT using SAM as a methyl donor.

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12
Q

What are the steps required for Tyrosine hydroxylase synthesis?

A

rate-limiting factor in catecholamines, TH is converted into DOPA using AADC into DA to make NE, you have to make DA first - converted from DA using a series of enzymes

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13
Q

How does Dopamine get converted into Norepinephrine

A

inside synaptic vesicles that have a membrane and transporter that brings in DA into the synaptic vesicle, dopamine is made in their cytosol; the presynaptic terminal vesicle has the enzyme DBH inside and converts inside vesicle cytosol

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14
Q

What are the main mechanisms for terminating the actions of catecholamines

A

Metabolism and Reuptake

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15
Q

Reuptake defintion?

A

Reuptake into presynaptic neurons via specific transporters

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16
Q

Metabolism degradation definition?

A

Metabolism degrades catecholamines that are not reabsorbed

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17
Q

What are the steps involved in serotonin synthesis?

A

Amino acid: tryptophan, enzyme converts to intermediary tryptophan hydroxylase
5 - hydroxytryptamine (5-HT)

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18
Q

What does PCPA do?

A

blocks serotonin synthesis, used in research

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19
Q

What is serotonin responsible for?

A

eating, sleeping, arousal, mood, mostly peripheral - 1-2% in the brain, found in the gut

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20
Q

What are the main amino acid neurotransmitters?

A

Glutamate, GABA, Glycine

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21
Q

How is GABA synthesized?

A

Glutamate is the precursor for GABA synthesis, GAD enzyme is responsible for converting glutamate to GABA, and requires pyridoxal phosphate (PLP)

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22
Q

What is retrograde signaling?

A

form of communication in the nervous system where signals are transmitted from the postsynaptic neuron back to the presynaptic neuron

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23
Q

What are examples of retrograde messengers?

A

Endocannabinoids, Nitric Oxide, Carbon monoxide

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24
Q

How do Endocannabinoids work as a retrograde messenger?

A

anandamide endogenous chemicals bind to brain receptor
CB 2: found in peripheral tissue, outside CNS
CB 1: all bind to the same receptors in the brain
dendrite gets excitable: makes endocannabinoids, releases & binds to receptor on presynaptic terminal, binding & activation of CB 1 receptors activates a gene protein, causing voltage-gated calcium channels to close
net outcome: block voltage-gated Ca channels stop neurotransmitter

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25
What is endomine's function?
pain and regulation of pain, 2 - AG; comes from neurons
26
How does Nitric Oxide work as a retrograde messenger?
relaxes vessels in brain, involved in learning/memory, pain volume transmission: on demand, no storage, no receptor, bulk transmission: released & go to neuron pass through the membrane internal changes: gene transcription, produced/secreted to bloodstream
27
How does Carbon monoxide work as a retrograde messenger?
relaxes brain blood vessels, regulate gastrointestinal motility
28
What are the endogenous THC-like neurotransmitters?
Anandamide 2-Arachidonoylglycerol
29
What is Anandamide's function
Binds to CB1 and CB2 receptors but has a higher affinity for CB1
30
what is 2-Arachidonoylglycerol's function
Binds to both CB1 and CB2 receptors
31
What is CB1?
located in the brain, responsible for neurotransmitter regulation and psychoactive effects.
32
What is CB2?
Located in immune cells, involved in immune response and inflammation
33
What is the most thoroughly studied transmitter-gated ion channel?
Nicotinic Acetylcholine Receptor: synaptic transmission and ion channels
34
What kind of channel mediates most of the fast synaptic transmission in the CNS?
Ionotropic receptors: ligand-gated ion channels: Glutamate and GABA
35
What are the three glutamate receptor subtypes?
AMPA NMDA Kainate
36
What is AMPA's function?
fast excitatory transmission in the CNS, Na⁺ and K⁺; glutamate binding
37
What is NMDA's function?
synaptic plasticity, learning, and memory, Na⁺, K⁺, and Ca²⁺, Glutamate
38
What is Kainate's function?
synaptic transmission and excitability, Na⁺ and K⁺, glutamate
39
In what important ways do AMPA and NMDA channels differ?
AMPA: mediates excitatory synaptic transmission, NMDA: ligand & depolarization
40
What does a “magnesium block” refer to and what is its importance?
extracellular Mg²⁺ ions block the NMDA receptor at resting membrane potentials
41
Which neurotransmitter mediates most synaptic inhibition in the CNS?
GABA - a main inhibitory neurotransmitter in the brain
42
Which ion passes through when its receptor channel opens?
Metabotropic: Slow Inhibition, Hyperpolarization
43
What types of drugs bind to GABAA receptors and how do they affect its function?
benzodiazepines - enhance the receptor’s function by increasing chloride ion (Cl⁻) influx, leading to hyperpolarization of neurons
44
What is the basic structure of G-protein-coupled receptors?
G-protein-coupled receptors (GPCRs) have a seven-transmembrane alpha-helix structure with an extracellular ligand-binding domain and an intracellular region that interacts with G proteins to trigger signaling pathways.
45
What is the basic mode of operation of guanosine triphosphate (GTP) binding proteins (G-proteins)?
G-proteins activate when GPCRs trigger GDP-GTP exchange, relay signals via the GTP-bound α-subunit, and deactivate when GTP is hydrolyzed to GDP.
46
What are the two types of effector proteins that activated G-proteins exert their effects through?
Activated G-proteins exert their effects through ion channels and enzymes
47
What are the Indolamines?
Serotonin Melatonin
48
What is melatonin's function?
regulation of the sleep-wake cycle, promotes sleepiness, made in the pineal gland Mostly used as a hormone, in the hypothalamus it can also function as a neurotransmitter hormones are released into the bloodstream, not the synaptic gap
49
What are Large molecule neurotransmitters (neuropeptides)
very diverse structures and functions made in the soma and transported in secretory granules away from the active zone of the presynaptic terminal. requires repetitive APs to build up Ca2+ to slowly release ribosomes making precursor peptides that gets converted into neuropeptides and cleaving happens in Golgi, which gets shipped out
50
What are Neuromodulators?
small molecules with characteristics unique from other neurotransmitters
51
What are Autoreceptors?
found on the presynaptic membrane Binds to neurotransmitter that is being released Dampens further release and induce hyperpolarization
52
Precursor example?
L-DOPA (Levodopa) to make dopamine
53
Cause synaptic release example?
Black Widow venom creates pores for Ca2+ in the presynaptic terminal thereby causing neurotransmitter dumping into the synapse
54
Agonist: Activate or enhance post-synaptic receptors example?
Morphine, THC, Nicotine, Ethanol, Benzodiazepines, Barbiturates
55
Inactivate pre-synaptic degradative enzyme examples?
initial class of antidepressants blocked monoamine oxidase (MAO)
56
Inactivate synoptic degradation enzyme example?
nerve gas, Sarin gas, insecticides, drugs inhibit acetylcholinesterase (AChE)
57
Blocks reuptake example?
cocaine, Ritalin, Adderall
58
What are the effects of L-DOPA on Parkinson's disease symptoms
Degeneration of substantia nigra dopamine neurons Central goal: Boost dopamine synthesis in the neurons that remain
59
What are the steps for L-DOPA
Steps: Tyrosine - TH enzyme - dopa - DOPA decarboxylase - DA
60
Prevent synaptic release example?
botulinum toxin, tetanus toxin
61
What is Optogenetics?
controlling the brain with light: Francis Crick Neurons don't respond to light - it is very specific and can be controlled Light can be precisely controlled: wavelength, intensity, pattern, on/offset Use of light-sensitive proteins from single-cell microbes to control neural activity