Test 1 Study Guide Part 3 Flashcards

1
Q

Cable properties:

  • Limit to diffusion distance:
  • Reason for limit:
A
  • 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)
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2
Q

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

A

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

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3
Q

What causes the spread of an action potential?

A

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

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4
Q

Action potentials in an unmyelinated nerve:

A
  • 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
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5
Q

Why do action potentials take longer in unmyelinated axons?

A

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.

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6
Q

The nodes and myelinated action potentials:

  • Conc. of Channels at nodes:
  • name of conduction:
A
  • Conc. of Channels at nodes:
    Much higher at nodes (but still present elsewhere)
  • name of conduction:
    Saltatory conduction (leaping conduction)
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7
Q

Conduction rates:

  • Myelinated axon:
  • Unmyelinated:
  • Reason aside from myelin:
A
- Myelinated axon:
100 m/s
- Unmyelinated:
1 m/s
- Reason aside from myelin:
Myelinated axons are also usually larger (less internal resistance)
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8
Q

Ca2+ roll in action potentials:

  • Disorders which are caused by hypocalcemia:
  • Reasons these disorders are caused:
A
  • 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.
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9
Q

Synapses:

  • cells synapses occur between in CNS:
  • cells synapses occur between in PNS:
  • Define effector cell:
A
  • 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)
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10
Q

Alternative name for neuron to muscle synapses:

A

Myoneural or neuromuscular junctions

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11
Q

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

A

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

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12
Q

What is necessary for electrical coupling of cells?

How is this accomplished?

A
Cells must be roughly equal in size and joined by a contact area of low electrical resistance.
Gap junctions (cells spaced 2 nanometers apart)
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13
Q

What is the structure of a gap junction?

A

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

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14
Q

Where are gap junctions localized?

A

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.

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15
Q

Are gap junctions adaptable systems?

A

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

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16
Q

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

A

CAMs (cell adhesion molecules)

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

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17
Q

Why do synapses act as one way gates?

A

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

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18
Q

What is a terminal bouton?

How large is the synaptic cleft?

A

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

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19
Q

What triggers the release of neurotransmitter into the synaptic cleft?

A

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.

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20
Q

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

A

SNARE complex

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21
Q

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

A

Synaptotagmin

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

22
Q

Which two SNARE proteins are complexed with the plasma membrane?

A

Syntaxin and SNAP-25

23
Q

Which SNARE protein is complexed with the vesicle membrane?

A

Synaptobrevin-2

24
Q

Voltage-gated channels:

Ligand-gated channels (chemically regulated channels):

A

Channels will be depolarizing or hyperpolarizing

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

25
Q

Graded changes:

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

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)

26
Q

How are EPSPs/IPSPs transmitted?

A

Cable properties

27
Q

Tell me the story of synaptic transmission:

A

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.

28
Q

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

A

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.

29
Q

Acetylcholine receptors:
Nicotinic:
Muscarinic:

A

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)

30
Q

Nicotinic ACh receptors:

Location:

A

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

31
Q

Muscarinic ACh receptors

Location:

A

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)

32
Q

Define
Agonist:
Antagonist:

A

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

33
Q

Antagonist of Muscuranic receptors:

Agonist of muscuranic receptors:

A

Antagonist: Atropine (belladona)
Agonist: Muscarine

34
Q

Antagonists of nicotinic receptors:

Agonist of nicotinic receptors:

A
Antagonist:
Curare
Alpha-bungarotoxin (from krait snake venom):
Agonist:
Nicotine
35
Q

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

A

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)

36
Q

How does the nicotinic acetylcholine receptor work?

A

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

37
Q

Tetrodotoxin mechanism of action:

A

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

38
Q

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

A

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

39
Q

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

A

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

40
Q

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

A

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

41
Q

Acetylcholinesterase:

  • location:
  • What it does:
  • Why it does it:
  • recycling:
A
  • 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
42
Q

Define Motor end plate:

Define end plate potential:

A

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

43
Q

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

A

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

44
Q

Curare:

  • Molecular mechanism (again):
  • Macrolevel effect:
A
  • 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
45
Q

What is the predominant neurotransmitter used by parasympathetic neurons?

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

A

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)

46
Q

Acetylcholine in the nervous system:

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

A

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

47
Q

Monoamines:

  • Define:
  • Examples:
A
- Define:
Regulatory molecules derrived from a single (mono) amino acid (amine)
- Examples:
From tyrosine:
Dopamine
Norepinephrine
Epinephrine
From histadine:
histamine
48
Q

Catechol:
Catecholamines:

A
Catechol:
a six carbon ring derived from tyrosine
Catecholamines:
Made from catechol (tyrosine)
e.g. dopamine, epinephrine, norepinephrine
49
Q

Seratonin:

- derived from ______:

A
  • derived from _____:

Tryptophan

50
Q

Histamine:

  • derived from ______:
  • What does histamine promote in the brain?
A
  • derived from ______:
    histadine
  • What does histamine promote in the brain?
    Wakefulness (which is why antihistamines can make you tired)
51
Q

Monamine oxidase:

  • Define:
  • What does it do:
A
  • 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.
52
Q

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

A

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.