Test 1 Study Guide Part 3

Question 1

Cable properties:

• Limit to diffusion distance:
• Reason for limit:

Answer 1

• Limit to diffusion distance:
  The ions can only diffuse 1 - 2 mm
• Reason for limit:
  High internal resistance (things in the way), external resistance (loss of charge to outside), high capacitance (charge must overcome stored charges by membrane)

Question 2

Why do multiple action potentials not deplete K+ or Na+ levels?

Answer 2

They happen over a very small localized reason on the surface of the nerve.
The Na+/K+ pumps run constantly, even through action potentials.

Question 3

What causes the spread of an action potential?

Answer 3

Cable properties. (which are in turn kept going because they stimulate new action potentials, which have new cable properties)

Question 4

Action potentials in an unmyelinated nerve:

Answer 4

• Continuous wave of action potentials down the length of the axon
• No loss of amplitude (or change in it) will result, so it is conducted without decrement

Question 5

Why do action potentials take longer in unmyelinated axons?

Answer 5

His reason: action potentials are slow relative to cable properties, so the fewer action potentials you can have the faster the conduction
Other reasons:
Myelin will decrease capacitance (less charge to overcome)
Myelin will decrease external resistance (less charge lost through efflux)
Myelinated axons are often larger, which results in less internal resistance.

Question 6

The nodes and myelinated action potentials:

• Conc. of Channels at nodes:
• name of conduction:

Answer 6

• Conc. of Channels at nodes:
  Much higher at nodes (but still present elsewhere)
• name of conduction:
  Saltatory conduction (leaping conduction)

Question 7

Conduction rates:

• Myelinated axon:
• Unmyelinated:
• Reason aside from myelin:

Answer 7

- Myelinated axon:
100 m/s
- Unmyelinated:
1 m/s
- Reason aside from myelin:
Myelinated axons are also usually larger (less internal resistance)

Question 8

Ca2+ roll in action potentials:

• Disorders which are caused by hypocalcemia:
• Reasons these disorders are caused:

Answer 8

• Disorders which are caused by hypocalcemia:
  Hypocalcemic tetany, and (neurological disorders in children)
• Reasons these disorders are caused:
  Lower interstitial Ca2+ results in less Ca2+ outside of the cell, This results in the outside being less positive, which depolarizes the membrane, making activation of Na+ channels in nerves easier.

Question 9

Synapses:

• cells synapses occur between in CNS:
• cells synapses occur between in PNS:
• Define effector cell:

Answer 9

• cells synapses occur between in CNS:
  Neurons and other neurons
• cells synapses occur between in PNS:
  neuron to neuron, neuron to effector cells
• Define effector cell:
  The cell which will respond to the stimuli (muscle cell or glandular cell)

Question 10

Alternative name for neuron to muscle synapses:

Answer 10

Myoneural or neuromuscular junctions

Question 11

What experiment did Otto Loewi perform to discover the chemical nature of some synapses?

Answer 11

He had two hearts, one still connected to the vagus nerve, suspended in baths with a pump which could circulate fluid between the baths.
With the pump off only the one connected to the vagus nerve slowed.
With the pump on both hearts slowed, indicating something diffusible, in our case acetylcholine.
He called it vagusstoff

Question 12

What is necessary for electrical coupling of cells?

How is this accomplished?

Answer 12

Cells must be roughly equal in size and joined by a contact area of low electrical resistance.
Gap junctions (cells spaced 2 nanometers apart)

Question 13

What is the structure of a gap junction?

Answer 13

Six proteins called connexins for a hemichannel (hemi = half, channel = channel)
Two hemichannels form a gap junction when docked together.

Question 14

Where are gap junctions localized?

Answer 14

Cardiac muscles, most smooth muscles

Gap junctions allow for quick dispersal of a signal unmodified between many cells. Examples:
In cardiac cells this allows the heart to beat in unison.
In smooth muscle cells, like those of the uterus, this allows contractions to occur to in unison.
The brain, where it is uncertain what they do.
Neuroglial cells where it is believed they allow exchange of Ca2+ and other ions.

Question 15

Are gap junctions adaptable systems?

Answer 15

Yes. The amount of gap junctions between cells can be changed to alter the conductivity.
They can also interact functionally with chemical synapses.

Question 16

What keeps post-synaptic and pre-synaptic extensions together?

Answer 16

CAMs (cell adhesion molecules)

These act like velcro to hold the synapses right where they need to be.

Question 17

Why do synapses act as one way gates?

Answer 17

There are only receptors for the neurotransmitter on side (post-synaptic). there is also, in theory, only production of neurotransmitter on one side.

Question 18

What is a terminal bouton?

How large is the synaptic cleft?

Answer 18

It is what idiots call the presynaptic endings (the end of axons).
Only 10 nms!

Question 19

What triggers the release of neurotransmitter into the synaptic cleft?

Answer 19

You know its the sweet release of Ca2+ into the pre-synaptic cell. Let me explain. The action potential depolarizes the cell, opening voltage gated Ca2+ channels, which enables a flood of Ca2+ in, which leads to release of neurotransmitter by fusing of synaptic vesicles remarkably quickly.

Question 20

What is the name of the protein complex which holds vesicles near the membrane walls?

Answer 20

SNARE complex

Question 21

Which protein complexes with Ca2+ and then the SNARE complex?
What does this lead to?

Answer 21

Synaptotagmin

Fuses the vesicles through a mechanism not entirely understood and releases their contents into the synaptic cleft.

Question 22

Which two SNARE proteins are complexed with the plasma membrane?

Answer 22

Syntaxin and SNAP-25

Question 23

Which SNARE protein is complexed with the vesicle membrane?

Answer 23

Synaptobrevin-2

Question 24

Voltage-gated channels:

Ligand-gated channels (chemically regulated channels):

Answer 24

Channels will be depolarizing or hyperpolarizing

Voltage-gated channels: Located primarily on the axon
Ligand-gated channels: Located predominately on the dendrites

Question 25

Graded changes:

• EPSP (Excitatory Post-Synaptic Potential):
• IPSP (Inhibitory Post-Synaptic Potential):

Answer 25

EPSP: Caused by an influx of Na+ (or any other cation)
IPSP: Caused by an influx of Cl- or efflux of K+ (or any other anion)

Question 26

How are EPSPs/IPSPs transmitted?

Answer 26

Cable properties

Question 27

Tell me the story of synaptic transmission:

Answer 27

An EPSP will build up to high enough levels in the dendrite or axon that the cable properties transmit to the initial axon segment. There the cable properties will start an action potential, which will conduct either by saltatory or normal conduction to the terminal bouton of the axon which will synapse with another cell 10 nm apart (its dendrite). SNARE is already prepped here, holding vessicles near the membrane. Ca2+ influx will result from the from the change in voltage. Ca2+ will complex with Synaptotagmin which will complex with the SNARE proteins (Two in the plasma membrane: Syntaxin, and SNAP-25, and one in the vessicle membrane: synaptobrevin-2) this results in the neurotransmitter entering the synaptic cleft. This will then diffuse to the next cell, and bind to ligand gated channels, causing a EPSP or IPSP which may result in an action potential. The number of impulses will convey strength of the stimuli, as well as the recruitment of neurons which have higher thresholds.

Question 28

Acetylcholine:
When is it always excitatory?
Where can it be excitatory or inhibitory?

Answer 28

ACh is excitatory for some neurons in the CNS and by somatic motor neurons in the neuromuscular junction.
At autonomic nerve endings ACh can be either excitatory or inhibitory.

Question 29

Acetylcholine receptors:
Nicotinic:
Muscarinic:

Answer 29

Nicotinic: are always excitatory and are used in the skeletal muscles. (nicotine is a poison which stimulates nicotinic receptors)
Muscarinic: can (muscurine is a poison which stimulates muscurinic receptors)

Question 30

Nicotinic ACh receptors:

Location:

Answer 30

Location: Autonomic ganglia, Skeletal muscle fibers, certain regions of the brain (addiction to nicotine)

Question 31

Muscarinic ACh receptors

Location:

Answer 31

Location:
Cardiac cells of the heart, smooth muscles, of particular glands and the brain. (It is therefore involved in the digestive system and cardiovascular system)

Question 32

Define
Agonist:
Antagonist:

Answer 32

Agonist: Causes activation of something when it binds
Antagonist: causes no activation when it binds (blocks agonists from binding)

Question 33

Antagonist of Muscuranic receptors:

Agonist of muscuranic receptors:

Answer 33

Antagonist: Atropine (belladona)
Agonist: Muscarine

Question 34

Antagonists of nicotinic receptors:

Agonist of nicotinic receptors:

Answer 34

Antagonist:
Curare
Alpha-bungarotoxin (from krait snake venom):
Agonist:
Nicotine

Question 35

Two methods of opening channels from a neurotransmitter signal, what are they:

Answer 35

Ligand-gated channels: The receptor is a channel, opens when bound (Nicotinic receptors are like this)
G-protein gated channels (like those used by muscuranic receptors)

Question 36

How does the nicotinic acetylcholine receptor work?

Answer 36

Acetylcholine binds to two of the five subunits.
This causes the channel to open.
Na+ and K+ can flow, but more Na+ flows because a stronger electrochemical gradient
The membrane is depolarized (EPSP) but cannot quite become positive (due to increased K+ permeability)
Ach binding is brief and it soon releases

Question 37

Tetrodotoxin mechanism of action:

Answer 37

Binds to voltage gated Na+ channels, inhibiting them (stops action potentials)

Question 38

Which do they block, action potentials or EPSPs. Why
Curare:
Tetrodotoxin:

Answer 38

Curare: blocks EPSPs because it inhibits nicotinic acetylcholine receptors (antagonist)
Tetrodotoxin: inhibits voltage gated Na+ channels, stops action potentials

Question 39

Muscuranic acetylcholine receptors as inhibitors (parasympathetic, IPSP inducers):
Where this occurs:
Describe the process:

Answer 39

Heart pacemaker cells (from vagus nerve [10th cranial nerve] stimulation, slows heart)

A single acetylcholine binds to the monomeric Muscuranic acetylcholine receptor
This causes a disassociation of the Alpha and beta-gamma subunits (Alpha releases GDP for GTP)
Beta-gamma complex acts to open K+ receptors which hyperpolarizes the cell, an IPSP

Question 40

Muscuranic acetylcholine receptors as promoters (sympathetic, EPSP inducers):
Where this occurs:
Describe the process:

Answer 40

The smooth muscle of the stomach

A single acetylcholine binds to the monomeric Muscuranic acetylcholine receptor
This causes a disassociation of the Alpha and beta-gamma subunits (Alpha releases GDP for GTP)
Alpha interacts with and disables K+ channels in the membrane
Decreased K+ efflux, the membrane depolarizes

Question 41

Acetylcholinesterase:

• location:
• What it does:
• Why it does it:
• recycling:

Answer 41

• location:
  plasma membrane of the postsynaptic cell or immediately outside of the synapse
• What it does:
  Acetylcholine -> acetate + choline
• Why it does it:
  Necessary to deactivate acetylcholine so stimulation stops
• recycling:
  Choline and acetate are recycled by the presynaptic cell, to make more acetylcholine

Question 42

Define Motor end plate:

Define end plate potential:

Answer 42

Define Motor end plate:
- postsynaptic membrane of a muscle cell
Define end plate potential:
An EPSP induced in a skeletal muscle fiber

Question 43

What results when a muscle cell is activated to a supra-threshold level by a nerve?

Answer 43

A process that is EXACTLY like an action potential, just on the surface of a muscle

Question 44

Curare:

• Molecular mechanism (again):
• Macrolevel effect:

Answer 44

• Molecular mechanism (again):
  antagonist of nicotinic acetylcholine receptors (competes with acetylcholine for binding sites but doesn’t activate receptors)
• Macrolevel effect:
  Flaccid paralysis, can be used as a muscle relaxant in medicine

Question 45

What is the predominant neurotransmitter used by parasympathetic neurons?

Give an example of a more sympathetic (activating) type of innervation involving muscaranic Ach:

Answer 45

Ach (through mechanisms like the vagus nerve, where beta-gamma subunits open K+ channels)

Activation of the stomach (remember this uses alpha subunits to inhibit K+ pumps)

Question 46

Acetylcholine in the nervous system:

- Is it in the nervous system, what does it do?

Answer 46

It induces EPSPs and IPSPs, acting exactly as we’ve learned it will act.

Question 47

Monoamines:

• Define:
• Examples:

Answer 47

- Define:
Regulatory molecules derrived from a single (mono) amino acid (amine)
- Examples:
From tyrosine:
Dopamine
Norepinephrine
Epinephrine
From histadine:
histamine

Question 48

Catechol:
Catecholamines:

Answer 48

Catechol:
a six carbon ring derived from tyrosine
Catecholamines:
Made from catechol (tyrosine)
e.g. dopamine, epinephrine, norepinephrine

Question 49

Seratonin:

- derived from ______:

Answer 49

• derived from _____:

Tryptophan

Question 50

Histamine:

• derived from ______:
• What does histamine promote in the brain?

Answer 50

• derived from ______:
  histadine
• What does histamine promote in the brain?
  Wakefulness (which is why antihistamines can make you tired)

Question 51

Monamine oxidase:

• Define:
• What does it do:

Answer 51

• Define:
  Breaks down monoamine neurotransmitters
• What does it do:
  Located in the presynaptic cell, it breaks down monamines as they are transported into the cell.

Question 52

What is the regulatory mechanism to remove monoamines from the synaptic cleft?

Answer 52

Monoamines are transported (by a reuptake transporter protein) back into the presynaptic cell
Monoamines are broken down by monoamine oxidase (MAO) in the cytosol of the presynaptic cell.