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+ CAPS 301: Neuro > Neurophysiology and NMJ > Flashcards

Neurophysiology and NMJ Flashcards

1
Q

Neuron

What is the input zone?

A

dendrites and cell body

part where incoming signals from other neurons are received

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2
Q

Neuron

What is the trigger zone

A

axon hillock

part where APs are initiated

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3
Q

Neuron

What is the conducting zone?

A

axon (1 mm to > 1 m long)

part that conducts APs in undiminishing fashion, often over long distances

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4
Q

Neuron

What is the output zone?

A

axon terminals

part that releases neurotransmitter that influences other cells

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5
Q

What cell types use electrical activity to perform their physiological roles?

A

neurons
cardiac myocytes
skeletal muscle cells
some secretory cells (ie. pancreatic 𝜷-cells)

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6
Q

What are excitable cells?

A

electrically active cells

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7
Q

How do excitable cells perform their physiological role?

A

harness difference in electrical charge between inside and outside of their cell membrane to function

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8
Q

Describe the different in charge between the inside and outside of excitable cells.

A

more negatively charged on inside than outside (0 mV outside)

electrical potential difference located immediately adjacent to cell membrane

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9
Q

What are the 2 initial conditions required for electrical activity?

A
  • selectively permeable cell membrane

- differential distribution across membrane of electrically charged ions in solution (Na+ and K+)

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10
Q

What is diffusion?

A

movement of solute (ie. ion) from area of high concentration to lower concentration by random thermal movement (no added energy needed)

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11
Q

How do ions (charged particles) diffuse through the membrane?

A

FACILITATED DIFFUSION

require path through the bilayer

ion channels in membrane provide path for Na+ and K+, etc.

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12
Q

Why can’t ions (charged particles) diffuse directly through the membrane?

A

not lipid soluble

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13
Q

What type of process is facilitated diffusion?

A

passive

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14
Q

Describe facilitated diffusion by means of conformation change.

A
  1. molecule to be transported binds to carrier (on binding sites exposed to ECF)
  2. carrier changes its conformation
  3. binding sites are now exposed to ICF, and transported molecule detaches from carrier
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15
Q

What is electrical activity in excitable cells important for?

A

neurons

cardiac and skeletal muscle

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16
Q

What is the distribution of K+ and Na+ inside and outside of the membrane?

A

K+ inside: 150 mM
K+ outside: 5 mM

Na+ inside: 15 mM
Na+ outside: 150 mM

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17
Q

How do cells concentrate K+ inside, and Na+ outside the cell membrane?

A

Na+ - K+ ATPase

  • pumps 3 Na+ out
  • pumps 2 K+ in

(uses ATP –> ADP)

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18
Q

What is the resting membrane potential (RMP)?

A

-70 mV

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19
Q

What is E_K+ and how is it established?

A

-90 mV

established by relatively large net diffusion of K+ outward

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20
Q

What is E_Na+ and how is it established?

A

+60 mV

relatively small net diffusion of Na+ inward neutralizes some of the potential created by K+ alone

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21
Q

Do large intracellular anionic proteins diffuse across the membrane?

A

no

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22
Q

What is permeability (or conductance)?

A

ease with which an ion can travel across membrane

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23
Q

How does permeability (P) include membrane voltage (Vm)?

A

greater P = greater Vm

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24
Q

What is the relative permeability of K+ : Na+ in most cells? Why?

A

~ 50 : 1

greater # of open K+ channels at rest (K+ leak channels)

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25
Q

What is depolarization?

A

Vm becomes more positive

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26
Q

What happens if you increase permeability of the membrane to Na+?

A

membrane potential shifts toward ENa (+60 mV) = depolarization

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27
Q

How can you depolarize the membrane? (3)

A
  • increase membrane permeability to Na+
  • decrease membrane permeability to K+
  • (theoretically) changing chemical gradient of Na+ or K+
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28
Q

What is hyperpolarization?

A

Vm becomes more negative

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29
Q

What happens if you increase permeability of the membrane to K+?

A

membrane potential shifts toward EK (-90 mV) = hyperpolarization

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30
Q

How can you hyperpolarize the membrane? (3)

A
  • decrease membrane permeability to Na+
  • increase membrane permeability to K+
  • (theoretically) changing chemical gradient of Na+ or K+
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31
Q

What determines membrane potential (Vm)? (2)

A
  • relative permeabilities of ions

- electrochemical gradient

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32
Q

What is an action potential?

A

large, all-or-nothing electrical event triggered when membrane potential reaches threshold

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33
Q

What occurs during an action potential?

A
  1. rapid membrane depolarization (due to increased Na+ permeability)
  2. rapid return toward resting membrane potential (due to increased K+ permeability)
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34
Q

Why is AP a regenerative event?

A

AP in one part of membrane will initiate AP in a more distant part of cell

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35
Q

What occurs at an AP subthreshold?

A

stimuli will not elicit AP → elicits graded potentials

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36
Q

What occurs at an AP suprathreshold?

A

stimuli will elicit AP of the same size, regardless of the magnitude of the stimulus

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37
Q

Components of Axonal AP

What is the initial depolarization?

How does it occur?

A

initial depolarization to AP threshold (not part of AP)

occurs in many ways, including EPSP, generator potential, and in lab by external stimulation

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38
Q

Components of Axonal AP

What occurs at the peak of AP?

Why?

A

Vm approaches ENa

far greater Na+ conductance (gNa) from open Na+ channels than K+ conductance (gK) resulting from open K+ channels

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39
Q

Components of Axonal AP

What occurs after hyperpolarization (AHP)?

Why?

A

Vm is closer to EK than at rest

K+ channels are open, and gK is greater than at rest

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40
Q

Where are generator potentials (GP) produced?

A

at sensory endings in periphery

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41
Q

Does a larger stimulus result in larger depolarization?

A

yes

GP is graded in amplitude - proportional to strength of the stimulus

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42
Q

When are APs produced?

A

if GP reaches threshold

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43
Q

What is the m-gate?

A

activation gate for Na+ channel

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44
Q

What is the h-gate?

A

inactivation gate for Na+ channel

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45
Q

What is the n-gate?

A

activation gate for K+ channel

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46
Q

Does K+ have an inactivation gate?

A

no

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47
Q

When do voltage-gated channels move their activation gate?

A

they have voltage sensor that moves in response to changes in membrane voltage

this movement is coupled to activation gate

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48
Q

How does depolarization influence the probability that the activation gate or inactivation gate is open?

A
  • increases probability that ACTIVATION gate is open

- decreases probability that INACTIVATION gate is open

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49
Q

What happens if either gate (activation or inactivation) is closed?

A

VG channel will not conduct

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50
Q

In what state are most VG channels in at rest?

A

available state

  • activation gate closed
  • inactivation gate open
  • channels are non-conducting, but ready to be activated by depolarization
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51
Q

What does a greater depolarization result in?

A

greater probability of getting all ions

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52
Q

Describe the positive feedback loop initiated by AP threshold.

A
  1. initial depolarization (ie. GP) opens some available VG Na+ channels in membrane
  2. Na+ influx (conductance) results in further membrane depolarization
  3. more depolarized membrane = increases probability that activation gate of available (but presently non-conducting) VG Na+ channels will open

loop repeats rapidly, opening all available VG Na+ channels

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53
Q

What are the 4 different phases of AP?

A
  • resting state
  • rising phase
  • falling phase
  • afterhyperpolarization (AHP)
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54
Q

Describe channel gating during resting state.

A

Na+ activation gate: closed (high prob.)

Na+ inactivation gate: closed (high prob.)

K+ activation gate: open (likely)

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55
Q

Describe channel gating during rising phase.

A

Na+ activation gate: open

Na+ inactivation gate: open

  • recovery from inactivation
  • channel is now in available state again
  • takes time

K+ activation gate: closed (likely)
- results in membrane returning to resting voltage

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56
Q

What happens when K+ activation gate closes?

A

results in membrane returning to resting voltage

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57
Q

What happens when Na+ inactivation gate opens?

A
  • recovery from inactivation
  • channel is now in available state again
  • takes time
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58
Q

Describe channel gating during falling phase.

A

Na+ activation gate: remains open
Na+ inactivation gate: closed
K+ activation gate: open

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59
Q

Describe channel gating during afterhyperpolarization (AHP).

A

Na+ activation gate: closed
Na+ inactivation gate: remains closed
K+ activation gate: remains open

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60
Q

Describe the rising and falling phases in the change in conductance of Na+ ions (gNa).

A
  • rising phase: Na+ channel opening

- falling phase: Na+ channels inactivating

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61
Q

Describe the rising and falling phases in the change in conductance of K+ ions (gK).

A
  • rising phase: K+ channel opening

- falling phase: K+ channels closing

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62
Q

What happens to gNa and gK during AHP?

A
  • gNa has returned to resting value

- gK is still elevated over resting values because K+ channels are still open

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63
Q

What is gNa and gK at rest?

A

not 0, but gK is significantly greater than gNa due to leak channels

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64
Q

What is the absolute refractory period?

A

period of time during which a second AP absolutely cannot be initiated, no matter how large the stimulus is

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65
Q

What is the relative refractory period?

A

interval immediately following the absolute refractory period during which initiation of a second AP is inhibited, but not impossible

(requires a greater stimulus intensity than the previous stimulus to generate AP)

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66
Q

Why does an AP fail to evoke during the absolute refractory period?

A
  • some Na+ channels are inactivated and cannot conduct current
  • still gK+ from open voltage-gated K+ channels (hyperpolarizing)
67
Q

What are the 2 types of AP propagation?

A

AP propagation combines both types:

  • passive (electrotonus)
  • active
68
Q

What is electrotonus?

A

passive process by which electrical events propagate

69
Q

What is current?

A

flow of + charge

70
Q

Where does current flow after entering neuron?

A
  • enters axon (or dendrite) of neuron through ion channels

- current will travel axially along resistive pathways of axon

71
Q

Describe the steps of electrotonus.

A
  1. triggering event opens Na+ channels → current enters axon (or dendrite) through ion channels in region of membrane and depolarizes it

inactive regions are at resting potential

  1. intracellular + charge is attracted to adjacent negatively charged regions of membrane → local current flow occurs between active and adjacent inactive areas (depolarizes inactive areas)
72
Q

What is electrotonic decay?

A

during electrotonus, charge leaks outward across the membrane as current travels along axon

73
Q

What does the length constant determine?

A

distance a passive electrical event (ie. depolarization) can propagate along a neuronal process

74
Q

How is the length constant calculated?

A

length constant = (Rm/Ra)^1/2

75
Q

What is the length constant?

A

ratio of axial resistance (Ra) and membrane resistance (Rm)

76
Q

How do you get a longer propagation distance.

A

larger length constant = longer propagation distance

increase length constant by:

  • increasing Rm
  • decreasing Ra
77
Q

How do you decrease Ra?

A

increase diameter of axon

78
Q

APs must travel along axons that are many times longer than their length constant (~0.1-1.0 mm). Electrotonus cannot do this. What is the solution?

A

active propagation

APs activate VG channels along axonal membrane to regenerate depolarization

79
Q

Describe active propagation in unmyelinated axon.

A

‘boosting’ with VG channels:

  • regenerates inward current
  • counteracts outward current leak
80
Q

What are the two variables that primarily influence rate of AP regeneration?

A
  • diameter of fibre

- amount of membrane capacitance

81
Q

How does the diameter of the fibre influence AP?

A

increase axon diameter = decrease axial resistance (Ra)

greater axial current flow provides more charge per unit time to neighbouring membrane segments

neighbouring membrane segments reach AP threshold more rapidly

82
Q

What is a capacitor

A

two conductive plates separated by insulating layer, that has ability to store electrical charge

83
Q

How does a capacitor work?

A

Vm gradually changes as charge separation across capacitor changes

changing charge on membrane surfaces (conductive plates of capacitor) during propagation of electrical potential takes time

84
Q

How does the amount of membrane capacitance influence AP?

A

less membrane capacitance = less time to charge membrane to threshold = greater rate of AP propagation

85
Q

What is the amount of capacitance proportional to?

A
  • proportional to surface area of membrane
  • inversely proportional to distance between parallel plates

specific capacitance of membrane is fixed (~ 1µF/cm2)

86
Q

How do axons reduce membrane capacitance?

A

by increasing effective thickness of membrane (distance between plates of capacitor) with a substance called myelin

87
Q

What is myelin formed from?

A
  • Schwann cells in PNS

- oligodendrocytes in CNS

88
Q

How does myelin affect AP?

A

APs can travel up to 50x times faster in myelinated fibres than in unmyelinated fibres

89
Q

Describe AP propagation between nodes of Ranvier.

A
  • AP travels electrotonically (passively)
  • membrane capacitance is lower
  • charge time of membrane is short
  • Rm is increased = longer length constant
  • depolarization propagates rapidly
90
Q

Describe AP propagation at nodes of Ranvier.

A
  • activation propagation
  • membrane capacitance is greater
  • charge time of membrane is longer
  • action potential slows
91
Q

What is a myelin sheath?

A

can have up to 300 layers of membrane

92
Q

Example: How is the stretch reflex activated?

A
  • AP travels along axon, into spinal cord
  • AP reaches axon terminal
  • AP depolarizes terminal
  • depolarization of terminus is converted into a release of chemical messenger, initiating synaptic transmission
93
Q

Where do synapses occur?

A

on cell body and dendrite of postsynaptic neuron

94
Q

Describe the steps of synaptic transmission.

A
  1. AP propagation in presynaptic neuron
  2. Ca2+ entry into synaptic knob
  3. release of neurotransmitter by exocytosis
  4. binding of neurotransmitter to postsynpatic receptor
  5. opening of specific ion channels in subsynaptic membrane
95
Q

Postsynaptic Membrane Effects

What does binding of a neurotransmitter to an extracellular receptor on a postsynaptic ion channel do?

A

induces conformation change of of channel, opening the channel pore

this allows ions to move across the membrane

96
Q

Postsynaptic Membrane Effects

What is generated as a result of ion movement through the pore in the postsynaptic cell membrane?

A

synaptic current (Isyn) is generated, which generates postsynaptic potential (PSP) - which is a change in Vm

97
Q

Postsynaptic Membrane Effects

What is excitatory postsynaptic potential (EPSP)?

A

change in membrane voltage of a postsynaptic cell following the influx of positively charged ions into a cell

98
Q

Postsynaptic Membrane Effects

How do EPSPs occur?

A

excitatory neurotransmitters bind to receptors that generate depolarizing PSPs, bringing Vm closer to AP threshold (EPSP)

99
Q

How many ions occupy a pore?

A

only one ion occupies the pore at any given moment

100
Q

Why can’t EPSPs fire in the postsynaptic neuron?

A
  • EPSP’s decrease in amplitude while travelling toward soma

- single EPSP will not bring neuron to AP threshold

101
Q

What do EPSPs need to do to cause AP firing in postsynaptic neuron?

A

EPSPs must summate

102
Q

What are the 2 types of summation?

A

temporal

spatial

103
Q

What is temporal summation?

A

involves repetitive activation of a single synapse

  • frequency is important – EPSPs must add together
104
Q

What is the result of temporal summation?

A

large compound EPSP results

  • compound EPSP may reach AP threshold at soma/axon hillock
105
Q

What is spatial summation?

A

involves simultaneous activation of multiple synapses

106
Q

What is the result of spatial summation?

A

large compound EPSP results

  • compound EPSP may reach AP threshold at soma/axon hillock
107
Q

What neurotransmitter do most excitatory synapses in CNS use to generate EPSPs?

A

glutamate

108
Q

What does glutamate (a neurotransmitter) act on?

A

may act on many receptor subtypes – two most common are AMPA and NMDA receptor-gated channels

109
Q

Glutamate and AMPA-gated EPSPs

What do AMPA-gated channels do?

A

allow both Na+ and K+ ions through open pore

  • this generates EPSP with equilibrium potential of ~0 mV
  • brings postsynaptic neuron closer to AP threshold
110
Q

Glutamate and AMPA-gated EPSPs

What happens to AMPA-gated and NMDA-gated channels when dendrites are at RMP?

A
  • AMPA-gated channel activation dominates EPSP generation
  • NMDA-gated channels blocked
  • fast EPSP
111
Q

Glutamate and AMPA-gated EPSPs

Example: What happens at relatively negative values of postsynaptic Vm?

A

glutamate binding activates AMPA receptor, which depolarizes the cell

BUT, Mg2+ blocks NMDA receptor

112
Q

What is inhibitory postsynaptic potential (IPSP)?

A

type of pSP that keeps Vm from reaching AP threshold (and therefore generating AP)

113
Q

How are IPSPs generated?

A

inhibitory neurotransmitters bind to receptors

114
Q

What is 𝜸-aminobutyric acid (GABA)?

A

common inhibitory neurotransmitter in CNS

  • there are several classes of GABA receptors
115
Q

What do GABA-A type GABA receptor-gated channels do?

A

allow entry of Cl- ions through open pore

  • inward movement of negative charge generates IPSP with equilibrium potential = ECl = -70 mV
  • note: in some cells ECl = RMP
116
Q

What physiological processes are skeletal muscles involved in?

A 
movement
breathing
GI tract activity (swallowing/defecating)
temperature regulation
speaking
venous/lymphatic fluid movement
protection of organs
117
Q

What does skeletal muscle activation require?

A

reliable and rapid transmission of signaling between nervous system and muscle cell

118
Q

What is the neuromuscular junction (NMJ)?

A

specialized synaptic contact between alpha motor neuron (a-MN) and muscle cell

119
Q

What does a motor neuron innervate?

A

one set of muscle fibres

120
Q

What is a motor unit?

A

functional unit consisting of a-MN and all muscle fibres (skeletal muscle cells) it innervates

121
Q

What is the motor unit for?

A

force generation

122
Q

Describe the structure of a motor unit, and explain how APs contract the unit.

A
  • a-MN axons can branch many times
  • each branch terminus innervates a single muscle cell (fibre) at NMJ
  • APs will travel down all branches of axon
  • a-MN APs simultaneously initiate excitation and contraction of each muscle fibre within motor unit
123
Q

What is a motor unit pool?

A

all of the motor units innervating a skeletal muscle

  • consists of many motor neurons, each of which innervates a motor unit within muscle
124
Q

What does the NMJ ultrastructure consist of?

A
  • presynaptic terminal
  • synaptic cleft
  • postsynaptic membrane
125
Q

Where is the NMJ formed?

A

at terminus of each branch of a-MN

126
Q

Where does NMJ usually contact muscle?

A

at mid-point along its length

127
Q

Describe how vesicles and peptide neurotransmitters travel from cell body to nerve terminal.

???

A
  1. vesicle and peptide neurotransmitter precursors and enzymes are synthesized in cell and are released from Golgi
  2. vesicles travel through axon on microtubule tracks via fast axonal transport - peptide neurotransmitters are already in some vesicles
  3. non-peptide neurotransmitters are synthesized and transported into vesicles in nerve terminal
128
Q

NMJ Ultrastructure - Presynaptic Terminal

What is the presynaptic termina?

A

distal part of a-MN and supportive Schwann cell

129
Q

NMJ Ultrastructure - Presynaptic Terminal

What is synthesized in the terminal?

A

ACh

130
Q

NMJ Ultrastructure - Presynaptic Terminal

Where is ACh stored?

A

in vesicles

131
Q

NMJ Ultrastructure - Presynaptic Terminal

How are vesicles organized?

A

into active zones close to synaptic membrane

132
Q

NMJ Ultrastructure - Presynaptic Terminal

How is ACh released?

A

via exocytosis by specialized machinery - SNARE proteins and Ca2+ sensor associated with each vesicle and underlying synaptic membrane

133
Q

NMJ Ultrastructure - Presynaptic Terminal

Where are ACh autoreceptors and when do they function?

A

present on terminal membrane

function during high frequency NMJ activation

134
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

What does the soma contain?

A

organelles and cellular machinery required to manufacture empty vesicles

135
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

What happens if soma dies?

A

results in denervation

136
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

What happens to severed axons?

A

may regenerate and re-establish functional NMJ

137
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

What is the soma required for?

A

health of axon

138
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

Where is ACh synthesized?

A

in presynaptic terminal

139
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

What is ACh synthesized from?

A

acetyl CoA and choline

140
Q

Presynaptic Terminal - a-MN and their Terminal Bouton

Where is ACh stored and transported?

A

stored in vesicles, which are then transported (fast axonal transport) to each axon terminal

141
Q

NMJ Ultrastructure - Synaptic Cleft

What is the synpatic cleft?

A

50 nm space between neuron and muscle cell

contains basal lamina (extracellular matrix)

??? adhesion and alignment of axon terminal active zones and muscle junctional folds

142
Q

NMJ Ultrastructure - Synaptic Cleft

Where is acetylcholinesterase (AChE)?

A

anchored within matrix, in close proximity to postsynaptic AChRs (ACh receptors)

143
Q

NMJ Ultrastructure - Postsynaptic Membrane

What do longitudinal junctional folds do?

A

provides large surface area for ACh receptor (AChR) activation

144
Q

NMJ Ultrastructure - Postsynaptic Membrane

What is at the ‘shoulders’ of each longitudinal junctional fold?

A

junctional AChRs are anchored, physically positioned opposite presynaptic active zones

145
Q

NMJ Ultrastructure - Postsynaptic Membrane

What is the perijunctional zone?

A

site of muscle AP initiation

146
Q

NMJ Ultrastructure - Postsynaptic Membrane

What does the perijunctional membrane have?

A

high density of VG Na+ channels

147
Q

NMJ Ultrastructure - Postsynaptic Membrane

What is found in non-junctional muscle membrane?

A

a second AChR type

more common during fetal development, during inflammation (ie. burn patients), and following denervation of muscle

148
Q

NMJ Chemical Transmission

Describe the sequence of transmission.

A

(generally same sequence as synaptic transmission)

  • each terminal branch of a-MN is simultaneously activated by axonal AP
  • AP activates VG Ca2+ channels in terminal bouton
  • vesicles containing ACh dock with synaptic membrane and exocytose ACh into synaptic cleft
  • ACh diffuses across cleft and binds to AChRs at postjunctional folds
  • AChRs open, allowing Na+ and K+ ions through pore, resulting in muscle membrane depolarization
  • AChE within basal lamina hydrolyses ACh into acetate and choline, terminating NM transmission
149
Q

Postsynaptic Junction Physiology

Where do EPPs propagate?

A

EPPs only need to propagate a short distance from postjunctional folds

150
Q

Postsynaptic Junction Physiology

What does the perijunctional region have a high density of? Why?

A

VG Na+ channels in membrane

ensures sarcolemma reaches AP threshold

151
Q

Postsynaptic Junction Physiology

Do EPPs normally reach AP threshold?

A

EPP is normally always large enough to reach AP threshold at perijunctional membrane (~40 mV in amplitude)

152
Q

Postsynaptic Junction Physiology

NMJ has a high safety factor. What does this mean?

A

every a-MN AP will result in muscle AP and subsequent contraction

153
Q

Presynaptic Effects

What are the two effects?

A
  • motor neuron cell body destruction

- demyelination

154
Q

Presynaptic Effects - Motor Neuron Cell Body Destruction

What does death of a-MN cell body cause?

A
  • paralysis, as axon degeneres and NM transmission blocked
  • loss of trophic factors released by presynaptic terminal – muscle atrophy

characteristic of polio viral infection

155
Q

Presynaptic Effects - Demyelination

What does destruction of a-MN axonal myelin do?

A

impairs AP propagation

  • can slow or block axonal APs
156
Q

Presynaptic Effects - Demyelination

What does AP slowing result in?

A

weakness, as motor units fire dis-synchronously

157
Q

Presynaptic Effects - Demyelination

What does AP blockade result in?

A

paralysis

158
Q

What are neuromuscular blocking agents (NMBAs)?

A

pharmacological agents used to block muscle contractions

159
Q

What are NMBAs used in?

A

surgical anesthesia

160
Q

NMBAs

What are the two types of muscle blockers?

A
  • depolarizing muscle blockers

- non-depolarizing muscle blockers

161
Q

NMBAs

How do depolarizing muscle blockers work?

A
  • activate AChRs and keep them open
  • membrane depolarizes and muscle contracts
  • prolonged AChR activation keeps muscle membrane depolarized
  • VG Na+ channels remain in inactive state
  • muscle APs are blocked and muscle cannot contract

ie. succinylcholine

162
Q

NMBAs

How do non-depolarizing muscle blockers work?

A
  • binds to AChR without opening channel
  • blocks ACh binding and prevents EPP production
  • no muscle AP = no muscle contraction

ie. rocuronium, tubocurarin

163
Q

NMBAs

What are non-depolarizing muscle blockers?

A

competitive antagonist of AChR

+ CAPS 301: Neuro (7 decks)

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