Synaptic Communication (Exam 1)

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Last updated 12:11 AM on 5/1/26
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58 Terms

1
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What is the resting membrane potential?

~ -70 mV

2
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What is the distribution of Na⁺ and K⁺?

Na⁺ high outside, K⁺ high inside

3
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What does the Na⁺/K⁺ pump do?

3 Na⁺ out, 2 K⁺ in (uses ATP)

4
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Where does the action potential (AP) begin?

Axon hillock

5
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What happens when the AP reaches the terminal?

Triggers neurotransmitter release

6
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What does AP arrival cause at the terminal?

Depolarization of terminal

7
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What channels open when the AP arrives?

Voltage-gated Ca²⁺ channels

8
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What enters the cell during neurotransmitter release?

Ca²⁺

9
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What is the role of Ca²⁺ in neurotransmitter release?

Triggers vesicle fusion

10
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Where do vesicles dock?

Active zone

11
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What are the key proteins involved in vesicle fusion?

SNARE proteins

12
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What is the function of SNARE proteins?

Pull vesicle → membrane

13
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What is exocytosis?

Vesicle fusion → neurotransmitter release

14
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What is endocytosis?

vesicle membrane removed fro cell membrane and recycle through local uptake

15
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Does the membrane build up during neurotransmitter release?

No

16
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How is the membrane recovered after neurotransmitter release?

Endocytosis

17
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What structure helps with vesicle recycling?

Endosome

18
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What is the size of the synaptic cleft?

20-50 nm

19
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How does the neurotransmitter cross the synaptic cleft?

Diffusion

20
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What happens after the neurotransmitter crosses the cleft?

Binds postsynaptic receptors

21
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Why is it important to clear neurotransmitters?

Prevent continuous activation

22
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What is the main method for clearing neurotransmitters?

Reuptake transporters

23
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What cells assist in neurotransmitter recycling?

Astrocytes

24
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What are glutamate and GABA converted into?

Glutamine

25
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What is the purpose of glutamine in neurotransmitter recycling?

Reused to make neurotransmitter

26
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What enzyme breaks down acetylcholine (ACh)?

Acetylcholinesterase

27
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What are the breakdown products of ACh?

Choline + acetate

28
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What happens to choline after ACh breakdown?

Reuptake → reused

29
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What is the effect of reuptake blockers?

Increase neurotransmitter in cleft

30
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What does cocaine block?

Dopamine, serotonin, norepinephrine

31
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What do SSRIs do?

Increase serotonin availability

32
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Where are receptors located?

Postsynaptic membrane

33
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What are receptors?

Membrane proteins with ligand binding site

34
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What is a ligand?

Molecule that binds receptor

35
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What are the two classes of receptors?

Ionotropic + metabotropic

36
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What is the mechanism of ionotropic receptors?

Direct ion channel

37
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How fast are ionotropic receptors?

Fast

38
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What is the duration of ionotropic receptor action?

Short

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What is the mechanism of metabotropic receptors?

G-protein → second messenger

40
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How fast are metabotropic receptors?

Slow

41
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What is the duration of metabotropic receptor action?

Long-lasting

42
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Can one neurotransmitter use multiple receptors?

Yes

43
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What determines the effect of a neurotransmitter?

Receptor type (not NT itself)

44
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What blocks NMDA receptors at rest?

Mg²⁺

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What removes the block from NMDA receptors?

Depolarization

46
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What ions pass through NMDA receptors?

Na⁺, Ca²⁺, K⁺

47
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What is EPSP?

Depolarization (Na⁺ in, usually glutamate)

48
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What is IPSP?

Hyperpolarization (K⁺ out or Cl⁻ in, usually GABA)

49
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What is spatial summation?

Multiple synapses at same time

50
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What is temporal summation?

Rapid repeated input from one synapse

51
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Where does summation occur?

Axon hillock

52
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What is long-term potentiation (LTP)?

Strengthened synapse after repeated activity

53
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What does LTP underlie?

Learning and memory

54
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Why does the balance of excitation/inhibition matter?

Maintains normal brain function

55
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What happens with loss of inhibition?

Overactivation (e.g., tetanus)

56
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What can too much excitation cause?

Epilepsy

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What other disorders are linked to excitation/inhibition imbalance?

Autism, schizophrenia

58
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Describe Tetanus

Bacteria that degrades SNARE proteins needed for vesicle exocytosis. Loss of inhibition results in uncontrolled motoe neuron activation and massive muscle contraction