Brainscape's Knowledge GenomeTM

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


See full index

PHGY 209 > Nerve Synapse > Flashcards

Nerve Synapse Flashcards

1
Q

Components of CNS

A

Brain and spinal cord

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

Components of PNS

A

Efferent fibers (motor neurons)
Afferent fibers (sensory neurons)
Autonomic fibers (for enteric nervous system)

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

Number of neurons in nervous system

A

100 billion neurons

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

How do neurons talk to each other

A

Communication takes place at synapses , which create neural networks

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

Characteristic structures of neurons?

A

Cell body (soma - contains the nucleus)
Dendrites (reception of soma)
Initial segment (insertion of axon into cell body)
Axon (enables communication with other neurons)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Flow of information?

A

Axons output onto dendrites
Flow down axon into presynaptic terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the resting membrane potential? What are the two contributing factors?

A

-60 to -70mV, caused by a small excess of negatively charged ions inside the cell
Concentration gradients & selective permeability to K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Concentration gradients for the various physiological ions

A

Na+ & Cl- going in
K+ & A- going out
A-= charged organic molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the K+ gradient

A

High permeability through leak channels (selective to K+)pulls K+ out of the cell
Creates an electrical gradient that pulls K+ back into the cell
When these two gradients are equal, the system is at equilibrium

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

What is the Nerst equation and why is it relevant?

A

Describes the membrane potential at equilibrium for each physiological ion - calculated based on ion flow in and out of cell
The dominant permeability is potassium at -90mV: the resting membran pot is higher due to a slight inward leak of Na+

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

Purpose of Na/K pump?

A

Maintenance of the Na and K gradients by ATP hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is and what’s the purpose of the action potential? Where does it start

A

Transient depolarizing spike moving down the axon
Propagation of information by brief electrical impulses
At the initial segment, propagating towards the presynaptic terminal

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

What is the threshold level of the action potential, what is it determined by?

A

The voltage that must be reached for the initiation of an action potential
Properties of ion channels in the axon membrane (especially voltage-gated sodium channels)

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

Voltage gated sodium channels: role, 3 properties

A

Cause the rising phase of the action potential by allowing for inward flow of Na
1) closed at resting membrane pot
2) selective to Na
3) Once open, rapidly inactivates

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

In what way is the rising phase of the action potential a regenerative process?

A

Positive feedback loop - the more the axon is depolarized, the more sodium channels open, the more the axon membrane is depolarized and so on

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

Voltage at the peak of the rising phase?

A

+30mV (near the equilibrium potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Compare the density of voltage gated Na channels and leak K channels

A

There are far more Na channels than leak K - the dominant permeability when the membrane is depolarized is for Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Voltage-gated K channels: role

A

Contributes to the falling phase by a delayed opening, allowing for K to flow out fo the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does action potential propagation work? (within an axon)

A

Spread of electrotonic currents (attraction of +30mV to -70mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the abolute refractory period?

A

the period where the membrane is completely inexcitable during sodium channel inactivation (right after the action potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the relative refractory period?

A

Point where the voltage of the axon membran overshoots its resting potential of -70mV : tremendously unlikely for the axon to be able to fire an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What specifies the information sent to the brain by an action potential (2)

A

By the frequence and pattern (timing) of their action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Effect of tetrodotoxin on sodium channels

A

Inhibitor - causes paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which naturally occuring neurotoxin affecting sodium channels causes paralysis

A

tetrodotoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Effect of batrachotoxin on sodium channels

A

Activator - causes seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which naturally occuring neurotoxin affecting sodium channels causing seizures

A

batrachotoxin

27
Q

List of 5 toxins that affect sodium channels (like the animals)

A

Pufferfish, frogs, scorpion, anemonae and insecticides

28
Q

Which drug class acts as anaesthetics, and how

A

____caine
by blocking sodium channels

29
Q

Antiepileptics, how do they work

A

Phenytoin and carbamazepine
by blocking sodium channels

30
Q

Why is rapid propagation of action potentials important for survival
What is one solution for this need
What is the propagation rate proportional to

A

-For situations that require rapid reflexive responses
-By making fatter ‘squid’ axons
-Propagation rate is proportional to axon diameter

31
Q

What is myelin, how is it formed

A

-insulator that raps around the axon
-formed of Schwann cells in the PNS or oligodendrocytes in the CNS

32
Q

Name of process speeding up action potential propagation in humans?

A

Saltatory conduction

33
Q

What is myelin’s role, name of gaps between it, how does it work

A

-increasing the conduction velocity of action potentials down the axon
-Nodes of Ranvier
-Bare regions between section of myelin have very high concentration of voltage-gated sodium channels, allowing for signal regeneration, preventing the electrical signal from fading

34
Q

What causes multiple sclerosis?

A

Loss of myelin - it can be regenerated but attacks generally also damage the axon during the strippage of myelin

35
Q

Where and what is white matter?

A

Inner section of brain and spinal cord, contains myelinated axons

36
Q

Where and what is grey matter?

A

Outer section of brain and spinner cord, contains cell bodies, dendrites and synapses

37
Q

What are the three main types of synapses? (one has two subclasses)

A

Axodendritic (onto a dendrite): spine or shaft synapse
Axosomatic (on soma, or cell body)
Axoaxonic (onto an axon)

38
Q

What are the two families of synaptic vesicles?

A

randomly distributed (floating in presnyaptic terminal)
docked vesicles (lined up in active zones)

39
Q

What triggers neurotransmitter release from the presynaptic terminal into the synaptic cleft?

A

Increase of calcium concentration via voltage gated calcium channels (closed at resting potential)

40
Q

What are the postsynaptic receptors?

A

Ligand-gated ion channels

41
Q

What triggers the opening of the calcium channels?

A

The action potential reaching the presynaptic terminal triggers the influx of calcium into the terminal

42
Q

What is the effect of the calcium influx into the terminal?

A

Synaptic vesicules fuse with the presynaptic membrane, releasing transmitter into the synaptic cleft

43
Q

Where does the neurotransmitter go after the synaptic cleft

A

It activates the receptors in the postsynaptic membrane

44
Q

Fundamental steps of chemical synaptic transmission?

A
  1. Action potential reaches presynaptic terminal
  2. Voltage gated calcium channels open
  3. Influx of calcium into terminal
  4. Neurotransmitter release into the synaptic cleft
  5. Activation of receptors by neurotransmitter in the postsynaptic membrane
45
Q

What are the two postsynaptic response to neurotransmitters?

A

Excitatory postsynaptic potential (EPSP) : depolarization
Inhibitory postsynaptic potential (IPSP) : hyperpolarization

46
Q

Main excitatory neurotransmitters?

A

Glutamate

47
Q

What are the two ionotropic glutamate receptors responsible for EPSP? How do they interact wiht neurotransmitters

A

AMPA and NMDA receptors - binding sites for the neurotransmitters, forming ion channels

48
Q

What is an ionotrpic receptor?

A

Ion channels that open in response to the binding of small molecules (e.g: neurotransmitters) to receptors on their external surfaces

49
Q

Role of AMPA receptors?
What ion do they permit transport of?
Result of their opening

A

-Responsible for “fast” EPSPs
-Na+
-Causes a small, short depolarization of the postsynaptic spine (-60mV to -58mV)

50
Q

How many EPSPs are necessary to initiate an action potential in the postsynaptic spine?

A

50-100, from multiple synapses acting in synchrony, or an individual synapse at high frequency

51
Q

Role of NMDA receptor?
How do they work?

A

-Contributes to the synaptic current by flow of Ca2+
-Pore is blocked by Mg+ until the membrane is depolarized: glutamate and glycine bind to receptors, allowing for a flow of Ca2+ into the postsynaptic spine

52
Q

What is synaptic plasticity?

A

The process of highly active excitatory synapses getting stronger (larger EPSPs) from NMDA receptors

53
Q

What is long-term potentiation?
Describe the three steps of the model?
What is the result?

A

A form of synaptic plasticity where NMDA receptors act as coincidence detectors between the events happening in the presynaptic terminal and the post synaptic spine.
1) Control : 1 action potential, measure EPSP strength
2) Burst of action potential, NMDA receptors activate
30 Hours after LTP induction (2), a single action potential provides a larger EPSP

54
Q

What occurs when neurons are in the presence of too high concentrations of glutamate?

A

A phenomenon called excitotoxicity: glutamate is generally cleard out very quickly (hence why EPSPs are so short) - under conditions where it remains (such a stroke, which releases glutamate from one neuron), there is a dangerously large influx of calcium into the cell, causing neuron death.

55
Q

What is the medical (global) consequence of excitotoxicity?

A

Neuronal degeneration (post stroke) or neurodegenerative diseases.

56
Q

Role (2) of inhibitory synapses?

A

-Shape excitatory signals
-Act as a break in excitation

57
Q

Main inhibitory neurotransmitter?

A

GABA

58
Q

Name of postsynaptic receptor responsible for IPSPs?

A

GABA(subscript)A receptors

59
Q

What ion do GABA A receptors select for?
What is the result in the postsynaptic spine?

A

Cl-
Hyperpolarization

60
Q

Synaptic integration (definition)

A

Totality of EPSP and IPSP inputs onto a cortical neruon, with information transmission (whether or not an action potential is fired) being dependent on the lreative balance between the two.

61
Q

role of metabotropic glutamate receptors (mGluR’s) // how do they work

A

Activated by the binding of glutamate, triggers a biochemical cascade, causing the diffusion of a chemical signal (by diffusion), called a second messenger to the inside of the postsynaptic spine.

62
Q

What are the roles of secondary messengers in the postsynaptic spine?

A

Activate a range of cellular porteins such as ion channels, protein kinases, transcription factors

63
Q

What are neuromodulators?
Where does the release of neuromodulators orginate from?

A

a messenger released from a neuron that affects the transmission of the signals between neurons
Small brainstem or midbrain nuclei

PHGY 209 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions