Week 3: Chemical Synapsis, Pharmacodynamics & Neurotransmitters Flashcards

1
Q

What is a synapse?

A

The site where a neuron contacts another cell to transmit information.

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2
Q

What is the synaptic cleft?

A

The small gap between pre- and post-synaptic cells where neurotransmitters diffuse.

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3
Q

What is a discrete synapse?

A

A type of synapse where neurotransmitters are released from terminal boutons at defined active zones.

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4
Q

What is a diffuse synapse?

A

A synapse where neurotransmitter is released from swellings called varicosities along the axon.

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5
Q

What determines neurotransmitter synthesis location?

A

Non-peptide transmitters are synthesized in terminals; peptides in the cell body.

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6
Q

How are neurotransmitters transported to terminals?

A

Via microtubules using kinesin-mediated anterograde transport.

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7
Q

What triggers neurotransmitter release at terminals?

A

Voltage-gated Ca2+ influx upon action potential arrival.

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8
Q

What proteins mediate vesicle fusion?

A

SNARE proteins facilitate docking and fusion of vesicles with the membrane.

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9
Q

What is synaptotagmin?

A

A calcium sensor that completes the SNARE complex to trigger fusion.

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10
Q

What causes synaptic delay?

A

Time needed for vesicle fusion and neurotransmitter diffusion and receptor binding (~0.5–1 ms).

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11
Q

Why are peptide synapses less efficient?

A

Require repetitive stimulation and have lower vesicle docking readiness.

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12
Q

What types of post-synaptic receptors exist?

A

Ionotropic (ion channels) and metabotropic (G-protein coupled).

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13
Q

What happens after neurotransmitter release?

A

It binds receptors, induces a response, and is then removed or degraded.

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14
Q

What ends neurotransmitter action?

A

Reuptake, enzymatic breakdown, or diffusion away from the cleft.

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15
Q

What is the difference between excitatory and inhibitory postsynaptic potentials?

A

Excitatory depolarizes the cell; inhibitory hyperpolarizes it.

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16
Q
A
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17
Q

What is pharmacodynamics?

A

The study of drug effects on the body.

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18
Q

What is efficacy in pharmacology?

A

The maximum effect a drug can produce (Emax).

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19
Q

What is drug potency?

A

The amount of drug needed to produce a specified effect (measured by EC50 or ED50).

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20
Q

What is binding affinity?

A

The strength with which a drug binds to its receptor (inverse of Kd).

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21
Q

What is a full agonist?

A

A drug that fully activates a receptor to produce maximum effect.

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22
Q

What is a partial agonist?

A

A drug that binds to and activates a receptor, but produces less than the maximal effect.

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23
Q

What is an inverse agonist?

A

A drug that reduces receptor activity below basal levels.

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24
Q

What is a competitive antagonist?

A

Binds to the same site as the agonist, blocking activation without triggering a response.

25
What is a non-competitive antagonist?
Binds elsewhere or irreversibly blocks receptor, reducing max response regardless of agonist concentration.
26
What is an allosteric modulator?
A molecule that binds at a site other than the active site and alters receptor activity.
27
What is the therapeutic index?
Ratio of TD50 (toxic dose) to ED50 (effective dose), indicating drug safety margin.
28
29
What is a graded dose-response curve?
A plot showing the range of drug effects across increasing concentrations.
30
What does EC50 indicate?
The concentration of a drug that produces 50% of its maximal effect.
31
What is Bmax?
Maximum receptor binding capacity.
32
What is Kd?
Dissociation constant; concentration at which 50% of receptors are bound.
33
What are spare receptors?
Receptors not required to achieve maximal response, indicating amplification.
34
What is a quantal dose-response curve?
A graph showing all-or-none responses across a population.
35
What does ED50 mean in a quantal curve?
The dose at which 50% of the population shows a defined effect.
36
What is TD50 or LD50?
The dose at which 50% experience toxicity (TD50) or lethality (LD50).
37
What is a therapeutic window?
Range of drug doses that are effective without being toxic.
38
How is drug safety evaluated?
By calculating therapeutic index (TI = TD50 / ED50).
39
Why is EC50 useful in dosing?
Helps determine effective and safe dosage levels.
40
What is the relationship between EC50 and potency?
Lower EC50 indicates higher potency.
41
What happens if EC50 < Kd?
Indicates presence of spare receptors in the system.
42
Why do partial agonists reduce full agonist effects?
They compete for receptors but yield smaller responses.
43
What is neutral antagonism?
A drug that binds without activating or altering baseline receptor activity.
44
45
What are the 3 main neurotransmitter classes?
Amino acids, amines, and peptides.
46
What qualifies a chemical as a neurotransmitter?
Synthesized and stored presynaptically, released on stimulation, and mimics synaptic effects when applied experimentally.
47
What is the main excitatory neurotransmitter in the CNS?
Glutamate.
48
What is the main inhibitory neurotransmitter in the CNS?
GABA.
49
What are the two glutamate receptor types?
Ionotropic (iGluRs) and metabotropic (mGluRs).
50
What are examples of ionotropic glutamate receptors?
NMDA, AMPA, and kainate receptors.
51
What are the two types of GABA receptors?
GABA_A (ionotropic) and GABA_B (metabotropic).
52
What neurotransmitter do cholinergic neurons release?
Acetylcholine (ACh).
53
What enzyme synthesizes acetylcholine?
Choline acetyltransferase (ChAT).
54
What breaks down acetylcholine?
Acetylcholinesterase (AChE).
55
What are the two cholinergic receptor types?
Nicotinic (ionotropic) and muscarinic (metabotropic).
56
What is serotonin also known as?
5-hydroxytryptamine or 5-HT.
57
How is serotonin synthesis regulated?
By availability of tryptophan, its dietary precursor.
58
What are serotonin receptor types?
Seven families (5-HT1 to 5-HT7) with diverse functions.
59
How is serotonin action terminated?
By reuptake into the presynaptic terminal via a specific transporter.