Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience (By Chapter) > Ch. 3: Synapses & Synaptic Transmission > Flashcards

Ch. 3: Synapses & Synaptic Transmission Flashcards

1
Q

Amount of NT release is proportional to:

A

number of action potentials arriving at presynaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 postsynaptic potentials

A
  • EPSP

- IPSP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clearing Synapse

A
  • Enzymes

- Reuptake Transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 types of synapses

A
  • Axodendritic
  • Axosomatic
  • Axoaxonic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

EPSP

A
  • Excitatory postsynaptic potential
  • Excitatory=depol
  • Na+ or Ca++ into cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

IPSP

A
  • Inhibitory postsynaptic potential
  • Inhibit=hyperpolarizes
  • Cl- in or K+ out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Presynaptic Facilitation

A
  • Always axoaxonic
  • “interneuron” stimulates presynaptic neuron to release more NT (by causing more Ca++ to enter)
  • Makes intended signal stronger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Direct Activation of Ion channels

A
  • Fast-Acting
  • Direct binding to ion channel
  • Quick open & short lived response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2 presynaptic potentials

A
  • Presynaptic Inhibition

- Presynaptic facilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A ligand can be a NT or neuromodulator based on:

A
  • where it is released

- Nuromodulator: not in synapse; released in extracellular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

NT

A
  • ligand released into synapse & binds to ligand-gated membrane receptor
  • Fast or slow based on what it binds to
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Presynaptic Inhibition

A
  • Axoaxonic

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

2nd Messenger

A
  • cAMP

- Used in indirect stiulation (g-protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

1st Messenger

A

NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Exogenous Ligands

A
  • NT produced outside the body

- Ex. Drugs/Meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Endogenous Ligands

A
  • NT produced in the body

- Ex. Glutamate

17
Q

Up Regulation

A
  • 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
18
Q

Down Regulation

A
  • Removal of post-synaptic receptors or turning off receptors
  • in response to high signal levels to decrease binding
19
Q

Antagonist

A
  • 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
20
Q

Agonist

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

- Ex. Nicotine is an Ach agonist

21
Q

7 events at synapse

A
  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)
22
Q

Neuromodulator

A
  • 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
23
Q

Indirect activation of ion channels

A
  • 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
24
Q

GABA

A

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

*Most prevalent fast acting inhibitory NT of CNS

25
Q

Ach

A

Location: PNS (at NMJ), ANS/CNS (fast)

Action: bind to ligand gated channel, EXCITATORY

26
Q

Glutamate

A

Location: CNS (Fast/slow)
Action: bind to ligand gated channel–EXCITATORY

*Most prevalent excitatory NT in CNS

27
Q

G-Protein receptor activation cause:

A

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

28
Q

G protein-mediated Receptors (with 2nd messenger)

A
  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
29
Q

Ligand-Gated Ion channels

A
  • Direct activation
  • NT binds to receptor on channel
  • Gate open and closes quickly
30
Q

2nd messenger system causes

A
  • Slow and prolonged change in cell function
  • membrane channels to open for long time
  • change Ca++ metabolism
31
Q

G-protein mediated receptors (indirect)

A
  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
32
Q

Myasthenia Gravis

A
  • 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

Neuroscience (By Chapter) (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions