Ch. 3: Synapses & Synaptic Transmission

Question 1

Amount of NT release is proportional to:

Answer 1

number of action potentials arriving at presynaptic terminal

Question 2

2 postsynaptic potentials

Answer 2

• EPSP

- IPSP

Question 3

Clearing Synapse

Answer 3

• Enzymes

- Reuptake Transporter

Question 4

3 types of synapses

Answer 4

• Axodendritic
• Axosomatic
• Axoaxonic

Question 5

EPSP

Answer 5

• Excitatory postsynaptic potential
• Excitatory=depol
• Na+ or Ca++ into cell

Question 6

IPSP

Answer 6

• Inhibitory postsynaptic potential
• Inhibit=hyperpolarizes
• Cl- in or K+ out

Question 7

Presynaptic Facilitation

Answer 7

• Always axoaxonic
• “interneuron” stimulates presynaptic neuron to release more NT (by causing more Ca++ to enter)
• Makes intended signal stronger

Question 8

Direct Activation of Ion channels

Answer 8

• Fast-Acting
• Direct binding to ion channel
• Quick open & short lived response

Question 9

2 presynaptic potentials

Answer 9

• Presynaptic Inhibition

- Presynaptic facilitation

Question 10

A ligand can be a NT or neuromodulator based on:

Answer 10

• where it is released

- Nuromodulator: not in synapse; released in extracellular fluid

Question 11

NT

Answer 11

• ligand released into synapse & binds to ligand-gated membrane receptor
• Fast or slow based on what it binds to

Question 12

Presynaptic Inhibition

Answer 12

• Axoaxonic

- “interneuron” inhibits more Ca++ influx so intended signal is weaker (because less NT released)

Question 13

2nd Messenger

Answer 13

• cAMP

- Used in indirect stiulation (g-protein)

Question 14

1st Messenger

Answer 14

NT

Question 15

Exogenous Ligands

Answer 15

• NT produced outside the body

- Ex. Drugs/Meds

Question 16

Endogenous Ligands

Answer 16

• NT produced in the body

- Ex. Glutamate

Question 17

Up Regulation

Answer 17

• Put more receptors on post-synaptic membrane or turn on receptors on post-synaptic membrane
• in response to decreased levels of NT, so there is increased binding

Question 18

Down Regulation

Answer 18

• Removal of post-synaptic receptors or turning off receptors
• in response to high signal levels to decrease binding

Question 19

Antagonist

Answer 19

• Substance that blocks NT action
• (blocks release of NT or binds to receptor so NT can’t bind)
• Ex. botox antagonist to Ach by blocking Ca++ channels–>NT not relseased

Question 20

Agonist

Answer 20

• Substance that acts like a NT & causes the same effect

- Ex. Nicotine is an Ach agonist

Question 21

7 events at synapse

Answer 21

1. action potential arrive at presynaptic terminal
2. depol opens Ca++ channels
3. Ca++ move vessicles to end of neuron
4. Vessicles bind with membrane and release NT
5. NT diffuse through synapse and bind to receptors
6. Binding initiates change
7. Clearing of synapse (enzymes/reuptake transporter)

Question 22

Neuromodulator

Answer 22

• Released outside synapse (extracellular fluid)
• bind to channels that slowly leak–partially depol cell so it facilitates the depol from the NT
• Modulates many neurons

Question 23

Indirect activation of ion channels

Answer 23

• Slow acting
• indirect binding to gated ion channel via receptor on g-protein
• channels open slower and have a longer response
• indirect activation of intracellular enzymes

Question 24

GABA

Answer 24

Location: CNS (fast or slow acting)
Action: INHIBITORY at ligand gated channels

*Most prevalent fast acting inhibitory NT of CNS

Question 25

Ach

Answer 25

Location: PNS (at NMJ), ANS/CNS (fast) Action: bind to ligand gated channel, EXCITATORY

Question 26

Glutamate

Answer 26

Location: CNS (Fast/slow) Action: bind to ligand gated channel--EXCITATORY *Most prevalent excitatory NT in CNS

Question 27

G-Protein receptor activation cause:

Answer 27

-Slow and prolonged opening and closing of ion channels using a second messenger

Question 28

G protein-mediated Receptors (with 2nd messenger)

Answer 28

1. NT bind to g protein receptor 2. GDP-->GTP 3. GTP complex binds to g-protein 4. increase production of ATP 5. ATP converted to cAMP 6. cAMP activates channels 7. complex inactivates and returns to start

Question 29

Ligand-Gated Ion channels

Answer 29

- Direct activation - NT binds to receptor on channel - Gate open and closes quickly

Question 30

2nd messenger system causes

Answer 30

- Slow and prolonged change in cell function - membrane channels to open for long time - change Ca++ metabolism

Question 31

G-protein mediated receptors (indirect)

Answer 31

1. NT binds to g-protein complec 2. GDP-->GTP 3. Complex to channel & binds to open channel (ions enter) 4. Complex inactivated and returns to receptor

Question 32

Myasthenia Gravis

Answer 32

- Autoimmune blockade or destruction of nicotinic Ach receptor on post-synaptic membrane--> - Decreased Ach binding (not enough receptors to bind Ach and recycle Ach to keep contraction going) - Treatment: Anti-cholinesterase to keep Ach in synapse longer