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physiology > NMJ MUSCLE ALL > Flashcards

NMJ MUSCLE ALL Flashcards

1
Q

Sequence of events from AP in a Motorneuron to AP in Sarcolemma of Muscle Cell

A
  1. AP travels along motoneuron axon
  2. AP invades motoneuron presynaptic terminal
  3. Ca 2+ influx in presynaptic terminal
  4. Vesicle fusion (exocytosis) with membrane of presynaptic terminal
  5. Release of Ach from fused vesicles
  6. Diffusion of ACh across neuromuscular cleft
  7. Binding of Ach to its receptors (AChR) in postsynaptic membrane (motor end plate)
  8. Opening of Na+ and K+ channels which are chemically regulated
  9. Na Influx and small K+ efflux across motor end plate
  10. generation of endplate potential
  11. opening of voltage-gated Na channels in sarcolemma immediately surroudning the motor endplate
  12. AP in sarcolemma
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2
Q

what is the site of regulation of skeletal muscle by the nervous system

A

NMJ

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3
Q

how many NMJ are found on most skeletal muscle cells

A

One NMJ on the surface membrane (sarcolemma)

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4
Q

how much space does the NMJ take up on the sarcolemma

A

less than .1%

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5
Q

specialization of the NMJ membrane

A

Highly specialized membranes (motor neuron and muscle)

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6
Q

the membrane of a muscle

A

Sarcolemma

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7
Q

where the neuron meets a muscle

A

Motor end plate

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8
Q

location of AChRs, and sodium channels in the post-synaptic membrane

A

ACHR’s are close to the motor nerve at the top of the secondary folds
Na Channels are at the bottom of the secondary folds

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9
Q

where is Acetylcholinesterase in the motor end plate

A

at the basin of the secondary folds near Na Channels

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10
Q

who has more complex motor end plates, adults are children

A

Adults

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11
Q

Comparison of the Neuromuscular cleft size to a vesicle at the NMJ

A

vesicle is 200 Angstrum

Cleft is 400 Angstrum

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12
Q

what causes a change in membrane potential at the motor endplate

A

ACh binding to its receptor following AP in motoneuron terminal

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13
Q

are changes in the endplate potential spontaneous

A

No

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14
Q

Are Endplate potential changes an all or none response

A

No, they are graded

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15
Q

Propogation of Endplate Potential

A

Do not propagate, contined to the end-plate region

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16
Q

Amplitude of Endplate Potential

A

about 10 mV (AP is 130 mV)

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17
Q

does changes in endplate POtential lead to AP

A

can undergo summation, but usually lead to an AP

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18
Q

what are miniature Endplate Potentials

A

Small endplate potentials

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19
Q

when do Miniature Endplate Potentials occure

A

spontaneously at rest

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20
Q

why do Miniature Endplate Potentials occur

A

Result from release of ACh from one vesicle

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21
Q

where do Mini endplate potentials occure

A

Confined to end-plate region

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22
Q

Amps of the Miniature Endplate Potentials

A

1-2mVc

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23
Q

Can Mini endplate Potentails do summation

A

Yes by the release of a few vesicles at the same time or in close proximity (both temporal and spatial)

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24
Q

what breaks do ACh

A

Acetylcholinesterase

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25
Q

location of Acetylcholinesterase

A

on the motor endplate membrane in the basal lamina

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26
Q

what results from the breakdown of ACh

A

Acetic acid (acetate) and Choline

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27
Q

what happens to the Acetic acid and Choline from the breakdown of ACh

A 
Acetate= circulation
Choline= presynaptic terminal, then reacts with acetyl-Coa by Choline acetyltransferase to form ACh again
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28
Q

effect of Curare

A

binds to AChR so ACh Cannot bind, causing ACh to still be released but not create an AP

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29
Q

where is Curare derived

A

Plant

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30
Q

effect of Botulinum toxin

A

blocks ACh release so skeletal muscle activation will not occur
- flaccid paralysis

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31
Q

effectof Organophosphates

A

Block action of AChE so ACh will not be hydrolyzed
Na channels remain in refractory state
- initially spastic paralysis
- end with flaccid paralysis

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32
Q

Organization of skeletal muscle

A 
whole muscle
Fascicle
Muscle fiber/cell
myofibril
Sarcomere
Filament
Protein
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33
Q

what makes up a thin filament in a muscle fiber

A

Two intertwined helical chains of actin molecules

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34
Q

what does tropoymosin and troponin associate with and there roll

A

Tropomyosin wraps around actin to block binding sites on actin
TRoponin is associeted with tropomyosin and binds to Ca to move tropomyosin and expose the binding sites on the tihin filaments

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35
Q

what makes up TRoponin

A

TnC - calcium binding
TnI
TnT - tropomyosin binding
subunites

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36
Q

what makes up a thick filaments

A

Myosin moleules

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37
Q

parts of a myosin molecules

A

Heavy chains
Light chanins
ATP binding sites
Actin binding sites

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38
Q

what is an iosform

A

same prootein but slightly different amino acid sequence; similar function

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39
Q

the functional unit of the contractile apparatus

A

Sarcomere

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40
Q

what is a sarcomere made of

A

Thick filaments
thin filaments
Z-lines

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41
Q

how many sarcomeres are in one muscle

A

Many

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42
Q

what is found the I band

A

Titin filament

Thin filament

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43
Q

what is the Titin filament

A

binds to the z line and the thick filament to elastically pull the sarcomere back together

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44
Q

what is found in the A band

A

thin filament
thick filaments
M line

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45
Q

what does the Z line bind

A

titin filament

thin filaments

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46
Q

what is found in the H zone

A

Thick filaments

M line

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47
Q

what does the M line bind

A

thick filaments

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48
Q

what is the border of a sarcomere

A

Z lines

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49
Q

roll of Nebulin

A

A molecular ruler to determine thin filament length

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50
Q

where is Nebulin found

A

Thin filament protein

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51
Q

what shape does thick filaments make around a thin filament

A

a triangle

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52
Q

what shape does thin filaments make around a thick filament

A

a hexagon

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53
Q

what is Excitation-Contraction coupling

A

Mechanism by which AP in sarcolemma initiates contraction

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54
Q

what ion has a pivotal role in activation of muscle

A

Ca

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55
Q

what does Excitation-Contraction copling do to Ca

A

a rapid and very large increase in free Ca

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56
Q

what binds to Ca2+ in the lateral sacs of the sarcoplasmic reticulum

A

Calsequestrin

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57
Q

EC coupling steps and release for Ca

A
  1. Muscle Action Potential propagate
  2. Ca released from the lateral sac of the Sarcoplasmic reticulum
  3. Ca binding to troponin removes blocking action of tropomyosin
  4. Ca removal from troponin restores tropomyosin blocking action
  5. Ca taken up by Sarcoplasmic reticulum using ATP
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58
Q

where is Ca ions released from the SR to initiate contraction

A

from the lateral sacs

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59
Q

what receptor tells the Sarcoplasmic reticulum to release Ca in responce to an AP

A

DHP receptor on the cell membrane interacting with the ryanodine receptor on the sarcoplasmic reticulum (same receptor allows ca to leave

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60
Q

where is the DHP receptor found

A

In the transverse tubules of the cell membrane

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61
Q

what makes up the DHP receptor

A

Ca++ channel and a voltage sensory

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62
Q

what makes up the sarcoplasmic reticulum

A

Lateral sacs and fenestrated collar

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63
Q

how is Ca ions sequestered/taken up by the sarcoplasmic reticulum

A

by the fenestrated collar sing the Ca ATPase pump in SR

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64
Q

what is the sliding filament theory

A

Muscle shortens by a relative sliding of thick and thin filaments
FILAMENTS DO NOT CHANGE LENGTH

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65
Q

what is the cross-bridge theory

A

thick and thin filaments are not connected at rest

cross-bridges form between the 2 types of filaments following an increase in Free Ca

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66
Q

relation of the cros-bridge theory and the sliding filament theory

A

cross-bridge theory is the mechanism of the sliding filament thoery

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67
Q

4 stages of Cross bridge cycle

A
  1. cross bridge binds to action
  2. power stroke due to relase of ADP and Pi from thick filament
  3. ATP binds to myosin and causes cross bridge to detach
  4. Hydrolysis of ATP energizes cross bridge
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68
Q

what is the amount of force generated by a sarcomere proportional to

A

number of attached cross bridges

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69
Q

what does the Rate of cross bridge formation determine

A

rate of muscle shortening

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70
Q

do all types of myosin go through the cycle at the same rate

A

No at different rates

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71
Q

of the cross bridge cycle, how many steps are attached and detached

A

2 attached

2 detaches

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72
Q

does a change in ATP concentration occur during muscle contraction and why

A

No, because the ATP conentration inside muscle cells is buffered by phosphocreatine

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73
Q

what does Phosphocreatine do

A

donates a phosphate to ADP to create ATP

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74
Q

what is the enzyme that allows PCr and ADP to make ATP

A

creatine kinase

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75
Q

where is creatine kinase found

A

at the M line

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76
Q

what are the 3 sources of ATP production

A

Creatine phophate
Glycolysis
Oxidative phosphorylation

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77
Q

what are the consumers of ATP

A

Myosin ATPase for contraction

Ca-ATPase for relazation

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78
Q

what is the length-tension relationship

A

amound of force that a muscle can generate is related to its length

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79
Q

how were the experiments done for the length tension relationship

A

activate muscle fiber
record tension
stretch
repeat

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80
Q

what is the ratio of how things are used for the sonsumption of ATP

A

70% contraction

30% relaxation

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81
Q

are thin fibers always the same in different fiber types

A

LEngths vary for different fiber types

Nebulin vary for differeny fiber types

82
Q

what does the the observation that a mscle can shorten at a higher veolcity when moving a lighter load

A

Velocity of skeletal-muscle fiber shortening and lengthening is a function of load

83
Q

how does the force being sustained by cross-bridges during a lengthening contraction compare to that of a maximum isometric tension

A

greater than the maximum iosmetric tension (can also lead to muscle injury)

84
Q

when does the maximum shortening velocity occure

A

with zero load

85
Q

when does the maximum isometric tension occur

A

with zero velocity

86
Q

formula for power

A

force x velocity

87
Q

is the max veolcity the same for all muscles

A

No, it is different for different types of skeletal muscles

88
Q

is the curvature of a velocity load graph the same for all skeletal muscle

A

Differs betwen types of skeltal muscle

89
Q

is the tension/cross sectional area the same for all skeltal muscle

A

Relatively constant

90
Q

isometric

A

Constant length

91
Q

Isotonic

A

constant load

92
Q

what happens to isotonic twitches as the load increases

A

slower velocity
lesss extent of shortening
greater latent periods

93
Q

muscle twitch

A

recaction of a muscle to one stimuli

94
Q

what is unfused tetanus

A

action of a muscle to multiple stimuli

higher tention than twitch but not always at a peak tension (shaking)

95
Q

what is fused tetanus

A

lots of stimuli

peak tension and constant

96
Q

what gives substrates to oxidative phosphorylation

A

products of glycolysis
fatty acids
oxygen
amino acids from protein (not normal though)

97
Q

what does the cell use to do glycolysis

A

GLucose from the blood and glycogen from the muscle fiber

98
Q

roll of glycogen more than just feeding glycolysis

A

keeps glucose concentration low in the cell so glocuse diffuses easily in

99
Q

what is a motor unit

A

a mingle motoneuron and all of the muscle fibers it innervates

100
Q

what is a single muscle made of

A

Many motor units

101
Q

how many NMJ does a muscle fiber have

A

one, with one motor neuron

102
Q

how many muscle fibers can one motorneuron innervate

A

more than one muscle fiber (100-2000) depending on fine or large movement muscle

103
Q

are motor units completely separated

A

no, they are intermingled

104
Q

how can muscle fiber types be distinguished

A

Structural (morphological)
Biochemical
physiological critera

105
Q

what may cause changes in the fibers that comprise a muscle

A

development disease

exercise

106
Q

Slow vs Fast fiber NMJ size

A

slow fibers have smaller SMJ

107
Q

diamter of slow vs fast muscles

A

slow fibers are smaller

108
Q

proteins found in slow vs fast muscle fibers

A

contain different sarcomere protein isoforms

109
Q

fatigue of slow vs fast fibers

A

slow are more fatigue resistant

110
Q

does the number of muscle fiber we have change after birth

A

no, but the types may change

111
Q

what source provides energy for fast fibers

A

More glycolysis

112
Q

what source provides energy for slow fibers

A

More oxidative phosphorylation

113
Q

type 1 fibers

A

Slow fiber

114
Q

types of type II fibers

A

type IIA

type IIB

115
Q

size of type IIA vs Type IIB fibers

A

type IIA are smaller

116
Q

does TYpe IIA or Type IIB do more oxidative metabolsim

A

type IIA more oxidative met

117
Q

are type IIA and IIB more fatigue resitsnat

A

Type IIA are more fatigue resistant

118
Q

what contracts slower type IIA or type IIB fibers

A

Type IIA are slower

119
Q

what generates more power, type IIA or type IIB

A

type IIB do more power (faster)

120
Q

efficiency of type IIA vs type IIB fibers

A

Type IIB are less efficient

121
Q

what type of fiber is the most efficient type of skeletal muscle

A

Type I is the most efficient

122
Q

what type of fiber is used to maintain posture

A

type I

123
Q

what type of fiber is used to do rapid, dexterous task

A

type II

124
Q

fatigure resistance of all 3 types of fibers

A

Type I: resistant
Type IIA: mediu resistant
Type IIB: Fatigue fast

125
Q

what are som systemic disorders associated with muscle cramps

A 
Dehydration
Metabolic
Endocrine
Pregnancy
Drugs/ toxins
126
Q

metabolic causes of muscle cramps

A 
Low sodium
Low Magnesium
Low calcium
Low Glucose
LowPotassium
127
Q

Endocrine disorders of muscle cramps

A

Thyroid (hyper or hypo)

Adrenal Insufficiency

128
Q

what kind of muscle is cardiac muscle similar to

A

Skeletal muscle

129
Q

length of cardiac sarcomeres

A

Not all the same length (possible functional consequences)

130
Q

what are cardiac sarcomeres composed of

A

Contractile proteins, that are in some cases also found in skeletal muscle

131
Q

major difference between cardiac and skeletal muscle

A

Cardiac has many more mitochondria

132
Q

size of skeletal vs cardiac muscle cells

A

Cardiac muscle cells are much smaller

133
Q

what allows conduction between myosites in cardiac muscle

A

Gap junctions

134
Q

benifit of cardiac muscle being different length sarcomeres

A

different sarcomeres allwyas at the max power potential (w/o would be compromised due to high filling)

135
Q

what does Skeletal muscle attach to

A

to tendons

136
Q

what does cardiac cells attach to

A

End on end to each other via an intercalated disk

137
Q

where are gap junctions locaetd

A

along each intercalated disk

138
Q

does the heart function as many units

A

one unit (quick passage of AP’s throughout ventricles

139
Q

what kind of synapse is found in the herat

A

Electrical synapses without chemical transmitters for AP transmission

140
Q

does mature skeletal muscle contain gap junctions

A

NO

141
Q

how does cardiac muscle get its energy

A

OXidative phosphorylation

142
Q

difference between cardiac muscle twitch and skeletal

A

cardiac and skelteal have very different tensions and APs for a twitch

143
Q

Refractory period length of a ventricular muscle cell vs skeltal

A

Ventricular is much longer(has a plateau period)

200ms vs 3ms

144
Q

importance of long refractory periods of Ventricular muscle cells

A

Prevents tetanis contractions (filling of hearting during diastole)

145
Q

how long does the AP of cardiac muscle last in relation to twitch tension compared to skeltal muscle

A

Cardiac: AP is until twitch tension is relaxed about 50%
skeletal: AP complete even before the muscle begins to shorten

146
Q

Stepts of the membrane potenetial of ventricular muscle

A 
depolarizing
Repolarization (brief and small)
Plateau (long and slow)
repolarization (brief and large)
Resting
147
Q

what flows in during the depolarization phase of Ventricular AP

A

Na flows into the cells

148
Q

what flow in during the 1st repolarization phase of Ventricular AP

A

K flows into the cell and Na leaves the cell

149
Q

what flows during the plateau phase of ventricular AP

A

Ca flows in and K leaves

150
Q

what flows during the secondar repolarization phase of ventricular AP

A

K flows in and Ca leaves

151
Q

what flows during the resting phase of a ventricular AP

A

No net current flow

152
Q

how does Ca get into heart muscle

A
  • Enter cells from interstitial space by passing through channels in sarcolemma during plateau pahse of AP
  • these Ca trigger other ca ions from SR that bind to troponin
153
Q

when Ca entering from the interstiticiul space cause release of Ca from the sarcoplasmic reticulum

A

calcium-induced calcium release

154
Q

when does Ca induced calcium release occure

A

during plateau phase of AP

155
Q

the primary mechanism for removal of Ca ions from the sarcoplasm

A

Ca-ATPase pump in the SR (just like that in skeletal muscle

156
Q

what is responsible for removing Ca out of the cell across the sarcolemma

A

Ca-ATPase pump

157
Q

what is the 3rd way to remove Ca from cardic muscle

A

Na/Ca exchanger moving Na inside cell and Ca out of the cell

158
Q

does the Na/Ca exchanger use ATP directly

A

No, uses secondary active transport from the Na concetration gradiant created by the Na/K ATPase

159
Q

what Ca removal mechansms move the amount of Ca out of the cell equal to the amount of Ca which moves in during the plateau phase of the AP during one contraction and relaxation cycle

A

sarcolemma Ca-ATPase

Na/Ca exchanger

160
Q

size of smooth muscle cells

A

very small (2-10 micrometers in diameter

161
Q

sarcoplasmic reticulum of smooth muscle

A

Little SR

162
Q

are there thick and thin filaments in smooth muscle

A

Yes, but not identical to skeletal and cardiac muscle

163
Q

what are the Z line homologes in smooth msucle

A

Dense bodies

164
Q

what do thin filaments attach to

A

Dense bodies

165
Q

what protein is not expressed in smooth muscle

A

Troponin

166
Q

what controls Smooth muscle

A

ANS (therefore involuntary

167
Q

what has a greater length range from which force can be generated, smooth or striated muscle

A

smooth

168
Q

why does smooth muscle need to contract at larger changes in length

A

accommodates large changes in volume of organs

169
Q

rate of ATP splitting by myosin in acivated smooth muscle and what the result of it is

A

10-100 times lower than skeletal so therefore no fatigue and better econmy

170
Q

what is the economy of muscle contraction

A

Force/ATP consumed

171
Q

what does Calcium bind to smooth muscle

A

Calmodulin

172
Q

EC coupling in smooth muscle

A
  1. stimulus increases calcium concentration
  2. caclium binds to calmodulin
  3. calcium calmodulin complex binds to inactive MLCK to create a Ca-Calmodulin MLCK active complex
  4. the Ca-Calmodulin-MLCK active causes Pi to bind to myosin leading to contraction
173
Q

what leads to the relaxed state of smooth muscle

A

phosphatase causeing Myosin-P to dissociate

174
Q

when is phosphatase active

A

caontinuously, but activation results when the MLCK activity is greater than the phosphatase activity

175
Q

roll of dephosphorylation in Contraction

A

dephosphorylation prevents reattachment of myosin to actin

176
Q

roll of ATP in smooth muscle contration

A

dissociation of myosin from actin as in striated muscle

177
Q

can dephosphorylated myosin bind actin

A

no

178
Q

what happens if myosin bund to actin in smooth muscle is dephosphorylated

A

remains attached in a rigor state with no movement of the cross-bridges

179
Q

Result dephosphorylated myosin reamining bound to actin

A

state of rigor with very little ATP consumption and high economy

180
Q

source of Ca for activation of smooth msucle

A

SR

Extracellular fluid

181
Q

sarcoplasmic reticulum in the Smooth muscle lack

A

No t-tubules

182
Q

what does the SR associate with in smooth muscle

A

Associate with the plasma membrane

183
Q

how is the SR activated in smooth muscle

A

that associated with the plasma membrane is released by an AP
non-membrane associated SR activated by second messengers

184
Q

how does Extracellular fluid Ca enter smooth msucles

A

from extracellular space through channels in plasma membrane

185
Q

what causes the rising phase of the AP of smooth msucle

A

inward flow of positive charge from Ca ions

186
Q

what is the resting potential of smooth muscle

A

never steady

187
Q

do smooth muscles need an neuron to create an AP

A

Some spontaneously generate APs

188
Q

what causes membrane potenetial to reach threshold in smooth msucle

A

Pacemaker potentials

189
Q

presence of neuromuscular junction for smooth muscle

A

No NMJ

190
Q

how does a neuron excite a smooth msucle

A

endings of motor neurons in ANS release neurotransmitters(excite or inhibit) near smooth muscle

191
Q

roll of hormones on smooth muscle

A

neurotrasmitters

192
Q

what local factors can influence smooth muscle

A

pH, oxygen level, nitric oxixde, stretch

193
Q

mechanisms of Ca removal

A

Ca pump in the sarcolemma
Na/Ca exchanger
SR

194
Q

types of smooth msucel

A

Singule unit

Multi-unit

195
Q

synapse in single-unit smooth muscle

A

Electrical synapses (gap junctions)

196
Q

how are single unit smooth muscles active

A

Spontaneously

197
Q

how are single unit smooth msucle activated

A

stretch activated

198
Q

innervation of single unit smooth muscle

A

primarily restricted to pacemaker cells

199
Q

examples of single unit smooth muscle

A

Smooth muscle in intestinal tract
uterus
small diameter blood vessels

200
Q

How is multi-unit smooth msucle activated

A

each cell is activated independently

Not spontaneous

201
Q

gap junctions in multi-unit smooth muscle

A

rare

202
Q

examples of multi-unit smooth muscle

A

Large arteries

Large airways

physiology (32 decks)

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