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Physio > Synaptic and Neuromuscular Transmission > Flashcards

Synaptic and Neuromuscular Transmission Flashcards

1
Q

Synpase

A

. Specialized connection btw neuron and receptor cell

. Presynaptic and postsynaptic regions and a space (synaptic cleft)

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2
Q

Electrical synapses

A

. Cell membrane of presynaptic and postsynaptic cells physically close in association
. APs transmitted directly via gap junctions
. No synaptic cleft
. NOT COMMON IN MAMMALS

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3
Q

Chemical synpase

A

. Electrical signal transmitted indirectly across cleft via chemical neurotransmitter
. STANDARD IN PEOPLE

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4
Q

Chemical synapse mechanism

A

. AP in presynaptic cell causes fusion of vesicles w/ membrane and release of neurotransmitter (NT) into cleft
. NT diffuses across cleft and binds to receptors on postsynaptic membrane
. Results in opening or closing of ion channel
. Change in ion channel activity causes graded potentials in postsynaptic cell that depolarize or hyperpolarize cell
. Delay seen btw pre and post cells due to chemicals having to diffuse and bind

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5
Q

Things that could happen to neurotransmitter floating around synaptic cleft

A

. Reuptake: taken up by presynaptic cell for recycling
. Diffusion: floats out of cleft
. Degradation: enzymes present in and around synapse degrade it
. Makes it so signal is present for a very short time in absence of further stimulation

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6
Q

Summation of signals

A

EPSPs and IPSPs need to sum together to reach threshold for firing APs

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7
Q

Integration of signals

A

. Input from multiple sources is combined through process of summation of large number of excitatory and inhibitory signals

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8
Q

Convergence of signals

A

Effect of large number of presynaptic neurons impinging on single postsynaptic neurons
. Most neurons receive input from many other neurons

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9
Q

Divergence of signals

A

. Single presynaptic neuron impinging on more than 1 postsynaptic neuron
. Normally is only 1 axon, but it may have collaterals that output onto a number of postsynaptic neurons

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10
Q

Physiological modulation

A

. Normal regulation of synaptic transmission
. Postsynaptic potentials can be variable in magnitude due to the changes in presynaptic and sometimes postsynaptic factors
. Much more common is presynaptic modulation

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11
Q

Presynaptic facilitation or inhibition is most often due to ____

A

. Changes in presynaptic Ca concentration that inc. or dec. vesicle fusion

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12
Q

Presynaptic facilitation

A

. Excitatory neurons impinging on presynaptic terminal or axon
. Inc. amt neurotransmitter released from presynaptic terminal

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13
Q

Presynaptic inhibition

A

Inhibitory neuron impinging on presynaptic terminal or axon
. Dec. amt of NT released from presynaptic terminal
. Impinging neuron has no direct effect on firing on postsynaptic neuron that is interacting with the neuron it is impinging on
. Only indirect effect by inhibiting the neuron it is impinging so there is no transmission to the final postsynaptic neuron

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14
Q

Modulation of synaptic transmission by drugs

A

. Every step in normal process can be enhanced or inhibited by drugs
. Most important sites of action for neurologically active drugs is synapses

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15
Q

How tetanus bacillus toxin interferes w/ motor neurons

A

. Stops inhibitory motor neurons of skeletal muscle so they are in constant activation
. Releases inhibitory transmitters from interneurons inn spinal cord causing no presynaptic transmission
. Causes proteolysis of SNARE proteins involved in fusion of synaptic vesicles to presynaptic plasma membrane

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16
Q

What kind of neuron excites skeletal muscle?

A

Alpha-motor neuron

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17
Q

Neuromuscular junction

A

. Motor axon terminals embedded in grooves in skeletal muscle fiber’s surface
. ACh-containing vesicles concentrated in active zone in synaptic terminal
. Active zones located over junctional folds in motor end-plate

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18
Q

Neurotransmitter in neuromuscular junction

A

. ACh
. Synthesized from choline and acetyl CoA via choline acetyltransferase (ChAT)
. Stored in vesicles in presynaptic terminal
. Found in active zone directly opposite moor end-plate

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19
Q

Exocytosis of ACh vesicles process

A

. Depolarization causes inc. in intracellular Ca via voltage-gated channels
. Inc. in Ca culminates in ACh release
. More intracellular Ca, more vesicles that fuse so more ACh released

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20
Q

Motor end-plate

A

. Specialized region of sarcolemma
. High contraction of ACh receptors (nicotinic cholinergic receptors)
. ACh-induced excitation of muscle fiber only happens here
. Have junctional folds to inc. surface area

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21
Q

Nicotinic cholinergic receptors

A

. Ligand-gated
. Several subunit form a pore
. 2 molecules ACh bind to alpha-subunits exposed on membrane surface
. Opens pore in portion of receptor embedded in lipid bilayer
. Na and K ions flow through open channel down electrochemical gradients

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22
Q

End plate potential (EPP)

A

. Channels opening in response to normal ACh release allow current to flow and depolarize end plate

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23
Q

Characteristics of EPP

A

. Graded
. Generated by mixed cation channel that is art of same protein as nicotinic receptors
. Conducts NA better than K so the equilibrium potential is near 0 mV

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24
Q

Effect of EPP

A

. Causes postsynaptic membrane potential to move towards 0mV
. Exhibits excremental conduction
. Augmented in amplitude and duration when rate of ACh degradation is dec. from drugs (negostigmine)

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25
Q

Margin of safety in EPPS

A

. Single neuronal AP can initiate postsynaptic (muscle) AP
. EPP can depolarize muscle by 50 mV, but only has to depolarize it 30 mV to reach threshold
. Beneficial in long term repetitive stimulation of presynaptic neuron as ACh release per AP declines from depletion
. Magnitude of EPP dec., but is still enough to make postsynaptic AP due to this safety

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26
Q

Relationship btw amplitude of EPP and muscle AP

A

. Normal 1:1 correspondence btw motor neuron AP and skeletal muscle AP
. Means that decision to excite muscular fiber is in CNS and is not modulated at neuromuscular synapse

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27
Q

Miniature end-plate potentials (MEPPs)

A

. At rest (no neuronal APs), single vesicles spontaneously fuse and release ACh into synaptic cleft
. Causes small depolarization (o.4 mV) of end plate
. Does not result in AP
. Occurs due to basal level of Ca in synaptic terminal
. Involved in trophies maintenance of functional integrity of neuromuscular junction

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28
Q

Modulation of neurotransmitter release in neuromuscular junction

A

. ACh amount released depends on available of ACh in immediate vesicle store and Ca concentration in synaptic terminal
. Level o dCa and ACh depends on amount of time btw successive depolarizations of terminal
. Minimum time needed for Ca and ACh to recover to pre-stimulation levels n

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29
Q

How alteration in ACh release effect neuromuscular transmissions

A

. Mild to moderate ACh alterations don’t affect normal muscle function due to EPP safety margin
. Facilitation of ACh release will inc. size of EPP, but EPP normally exceeds threshold for AP anyway
. Take large depression of ACh release due to large safety
. Comes into play in disorders that decrease safety and ACh and Ca levels matter more

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30
Q

Lambert-EatonSyndrome

A

. Complication of cancers, esp small-cell carcinoma in lung
. Weakness from dec. ACh release in motor nn from dec. Ca channels
. Patient blood has high antibodies to Ca channels causing destruction of them
. Immunosuppressants relieves symptoms

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31
Q

Ca-triggered vesicle fusion mechanism

A

. SNARE proteins on synaptic vesicle and plasma membrane complex together and fuse
. Ca binds to synaptotagmin on vesicle membrane
. Cytoplasmic region of protein inserts into plasma membrane and catalyzes membrane fusion

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32
Q

Structure of SNARE complex

A

. Vesicular synaptobrevin form helical complex w/ syntaxin and SNAP-25

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33
Q

Botulism

A

. Group of toxins from Clostridium botulinum bacteria
. Causes muscle weakness and paralysis by interfering w/ ACh release
. Can cause respiratory failure
. Degrades SNARE so it is preferential to ACh and skeletal muscle
. Can be some smooth muscle dysfunction as well

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34
Q

Myasthenia Gravis

A

. Unable to maintain prolonged contraction of skeletal muscles
. Starts in eyelids
. Patients have antibodies to nicotinic receptor on skeletal muscles from autoimmune response
. Motor neurons less likely to cause postsynaptic muscle cells to reach threshold
. Treatment: cholinesterase inhibitors

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35
Q

What occurs in skeletal muscle if there is an insufficient supply of ATP

A

. Myosin can’t dissociate from actin, cross bridge remains intact

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36
Q

T/F rigor mortis represents maximal contraction

A

F

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37
Q

Ca-ATPase role in skeletal muscle contraction

A

. In sarcoplasmic reticulum
. Actively transports Ca ions into sarcoplasmic reticulum which lowers free Ca concentration
. This terminates contraction and allows muscle fiber to relax
. ATP hydrolysis provides energy to transport Ca

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38
Q

What determines maximal muscle contraction velocity?

A

. Rate of ATP hydrolysis determined rate of cross-bridge cycling

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39
Q

WHat is one of the most important factors influencing speed of cross-bridge cycling and sarcomere shortening?

A

. Isoform of MHC expressed in muscle fiber

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40
Q

Which type of muscle fibers have an isoform of myosin ATPase that splits ATP to ADP and P quickly?

A

Fast-twitch muscle fibers

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41
Q

T/F there is only one neuromuscular junction per muscle fiber

A

T

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42
Q

Where is the neuromuscular junction located in muscle fiber?

A

Near the middle of fiber so AP can spread equally to both sides

43
Q

The amount of ACh that is normally released during AP opens ____ ion channels in motor end plate?

A

400,000

44
Q

ACh receptors

A

. On postsynaptic membrane
. Nicotinic
. Ligand-gated, cation-selective (Na, K, Ca)
. Open upon ACh binding

45
Q

Acetylcholinesterase

A

. Degrades ACh
. Located in postsynaptic membrane
. Choline taken back into presynaptic motor nerve terminal for resynthesis of ACh

46
Q

Transmission at neuromuscular junction

A

. AP generated in motor neuron
. Depolarization of neuron axon terminal opens voltage-gated Ca channels, Ca moves into acorn terminal
. Exocytosis of ACh-containing vesicles (# dependent on Ca concentration in n. Terminal
. ACh diffuses to ACh receptors on motor end-plate of muscle membrane (in junctional folds of sarcolemma)
. ACh binds to receptor causing large cationic influx (mostly Na) and small K efflux generating depolarizing EPP
. EPP generate AP in muscle membrane
. Acetylcholinesterase breaks down remaining ACh in neuromuscular junction to prevent continued contraction

47
Q

SKeletal muscle resting membrane potential

A

. potential has large contribution to Cl conductance along with K
. Value is more negative in muscle than neurons

48
Q

Skeletal muscle action potential

A

. EPP produces local inward current flow at motor end plate
. Initiates AP in muscle membrane that propagates over surface of muscle fiber
. Na current through voltage-aged Na channels generates upstroke of AP in muscle membrane
. K current generates repolarization of muscle membrane

49
Q

How black widow spider venom alters release of ACh

A

. Causes explosive release of ACh

50
Q

How clostridium botulinum toxin alters ACh release?

A

. Blocks ACh release

51
Q

How lambert-Eaton syndrome alters release of ACh

A

. Self-producing antibodies to Ca channels diminish Ca influx into presynaptic terminal during AP
. Reduces ACh release

52
Q

How curare bloack ACh receptor site

A

Reversible binds to ACh receptor sites

53
Q

How myasthenia Gravis blocks ACh receptors

A

Self-produced antibodies that inactivate ACh receptor sites

54
Q

How organophosphates prevent inactivation of ACh

A

. Irreversibly inhibits acetylcholinesterase

55
Q

Excitation-contraction coupling

A

. Series of events linking electrical phenomena occurring in plasma membrane to cell shortening that causes muscle contraction
. Delay (latent period) btw electrical signal and mechanical response represent excitation-contraction coupling

56
Q

Transverse tubules

A

. Invaginations in sarcolemma
. Conduct AP rapidly to center of cell
. Results in homogenously synchronic muscle contraction
. Flanked by terminal cisternae

57
Q

Terminal cisternae

A

. Sack-like structures
. Store and release Ca for contraction
.

58
Q

Longitudinal portion of sarcoplasmic reticulum in skeletal muscle significance

A

Forms network where Ca-ATPase-mediated Ca reuptake takes place

59
Q

Role of Ca in skeletal muscle contraction

A

. SR is sole source of Ca
. Needed for cross-bridging
. As long as Ca and ATP are available, cross-bridge cycling continues
. When SR removes Ca from muscle cytoplasm relaxation occurs

60
Q

Slow oxidative fibers

A 
.red
. Oxidative phosphorylation primary ATP source
. Many mitochondria 
. High myoglobin content 
. Low glycogen content 
. Slow rate of fatigue 
. Slow contraction velocity 
. Small fiber diameter 
. Small motor unit size 
. Small size of motor neuron innervating fiber
61
Q

Fast oxidative glycolytic fibers

A

. Red
. Oxidative phosphorylation primary source of ATP
. Many mitochondria
. High myoglobin content
. Intermediate glycogen, rate of fatigue, contraction velocity, fiber diameter, motor unit size, and size of motor neuron innervating fiber

62
Q

Fast glycolytic muscle fibers

A 
. Glycolysis primary source ATP 
. Few mitochondria 
. Low myoglobin
. High glycogen 
. Fast rate of fatigue 
. Fast contraction velocity 
. Large fiber diameter, motor unit size, and size of motor neuron innervating fiber
63
Q

Muscle tension

A

. Force exerting on an object by a contracting muscle

64
Q

Types of muscular contraction

A

. Isotonic
. Isometric
. Lengthening

65
Q

Isotonic contraction

A

. Muscle tension remains constant as muscle length changes
. Occurs when muscle shortens causing load to be moved
. Also called concentric contraction
. Muscle tension is greater than opposing load

66
Q

Isometric contraction

A

. Static
. Muscle is prevented from shortening so tension develops at constant muscle length
. Occurs when muscle supports load in constant position (doesn’t move)
. Muscle tension is equal to the opposing lead

67
Q

Lengthening contraction

A

. Load pulls muscle to longer length in spite of opposing force being produced by cross bridges
. Eccentric contraction
. Lengthening of muscle fibers is consequence of external force being applied
. Muscle tension less than opposing load

68
Q

Latent period in skeletal muscle

A

. AP in skeletal muscle lasts less than 5 ms
. Onset of contractile response lags behind AP due to entire process of excitation-contraction coupling must take place before cross-bridging begins

69
Q

Summation of skeletal muscle contractions

A

. Ca removal from cytoplasm takes time
. Inc. in muscle tension from successive APs during phase of mechanical activity
. Tension is summated, not voltage
. APs don’t summate, muscular contractions do

70
Q

Maximal force of contraction is reached with what kind of tetanus?

A

Fused tetanus

71
Q

Tetanus mechanism

A

. Sustained contraction where individual twitches aren’t distinguishable from each other
. Single twitch cytosolic Ca levels remain elevated after AP terminates, 2nd AP excites muscle during this period and more Ca released further inc. Ca concentration
. Resulted in larger muscle tension

72
Q

T/F Each AP always produces same amount of SE release, which is the max amount

A

T, Ca release from SR is not regulated

73
Q

How maximal muscle tension occurs

A

. Single AP doesn’t produce it
. When APs come at high frequency, the basal Ca concentration rises, inc. total cytosolic Ca concentration during summation
. If cytoplasmic Ca concentration remains high, maximal tension will develop

74
Q

T/F fast glycolytic fibers tetanize at higher frequency than slow fibers

A

T

75
Q

What is the optimum muscle length?

A

Resting length

76
Q

What happens when muscles are overstretched?

A

. No overlap btw actin and myosin

. Cross-bridging can’t occur

77
Q

What happens when muscles are overshortened?

A

. Actin and myosin physically overlap

. Interferes w/ cross-bridge formation

78
Q

Force-velocity relationship

A

. Contraction properties depend on amount of load
. Smaller load: larger shortening, faster muscle contractions
. At lower loads, muscle tension generates isotonic shortenings
. When load exceeds tension, lengthening contraction occurs

79
Q

Motor units

A

. Motor neuron plus muscle fibers it innervates
.When AP happens, all muscle fibers in motor unit contract
. Muscle fibers of unit are always the same type
. Motor unit size depends on muscle function
. Fine motor control: smaller units

80
Q

Motor unit recruitment

A

. Inc. number of motor units that are active in a muscle
. Determines total tension that a muscle can develop
. Motor units w/ lowest threshold activate first, then recruitment progressively add motor units
. Results in greater force production

81
Q

Most excitable motor units are what kind of fibers?

A

Slow oxidative fibers

. Found in fine-movement muscles and in muscles used for continuous movements

82
Q

Least excitable motor unit muscle fiber type?

A

Fast glycolytic fibers

. Activated during high intensity activity when quick bursts of power are needed

83
Q

Size principle with skeletal muscle

A

. Small motor units activated first
. Progresses to more difficult to excite, more powerful large motor units
. Small units: small motor neurons, conduct APs slowly and excite fewer fibers that are slow twitch type
. Large units: large motor neurons, conduct APs rapidly and excite many fibers that are fast twitch type

84
Q

Graded force production in skeletal muscle is primarily determined by ____

A

. AP frequency w/ summation of contractions

. Recruitment of motor units

85
Q

Number of fibers per motor units determines what relationship?

A

. Frequency-tension relationship (AP frequency w/ summation)

86
Q

Number of active muscle fibers determines ___

A

Tension developed by each individual fiber

87
Q

Number of active motor units (recruitment) determines that relationship?

A

Length-tension relationship (fiber length)

88
Q

Sources of energy for skeletal muscle

A

. Phosphocreatine: enzyme creatine phosphotransferase tranfers P to ATP reforming ATP
. Glycogen: degraded to pyruvate then lactate for anaerobic glycolysis
. Pyruvate: w/ oxygen, enters TCA for oxidative phosphorylation

89
Q

Muscle fatigue

A

. Process to replenish energy stores takes energy
. Muscle consumes O at inc. rate (O2 debt) for some time after activity has stopped to replenish energy stores
. When muscle repeatedly stimulated, the max tension produced dec. (fatigue)
. Dec. shortening velocity
. Slower rate of relaxation

90
Q

Growth of skeletal muscle

A

. Growth is adding new myofibrils w/in a cell, formation of new cells, or adding more sarcomeres in series as muscle cells lengthen along w/ skeletal growth

91
Q

Muscle hypertrophy

A

. Addition of myofibrils inc. muscle mass
. Adds sarcomeres parallel
. Inc. size of individual muscle fibers inc. force
. Short duration high intensity inc. fast glycolytic fibers
. Low intensity long duration produces changes in slow oxidative and fast oxidative-glycolytic fibers, but only limited hypertrophy
. Muscle fibers in men are thicker and larger from androgenic steroid hormones in higher concentrations

92
Q

Muscle atrophy

A

. Disuse

. Enervation: motor neurons destroyed

93
Q

Muscular dystrophy

A

. Structural defects of cytoskeletal proteins can lead to group of muscle disorders
. Characterized by weakness and muscle mass loss

94
Q

Muscle hyperplasia

A

. Number of muscle fibers inc.
. Skeletal m. Has limited ability to form new fibers
. Happen from differentiation of satellite cells present in tissues
. Can occur as result of high volume moderate intensity weightlifting protocol used by some bodybuilders
. Overall contribution to muscle size and strength is minimal

95
Q

Muscle postnatal growth

A

. Muscle growth in kidneys occurs by lengthening and hypertrophy

96
Q

External causes of muscle damage

A

. Contusions/crushing
. Laceration
. Extreme heat or cold

97
Q

Internal causes of muscle damage

A

.muscle tears: accompanied by bleeding into muscle belly
. Extreme/unaccustomed exercise: due to eccentric contraction, high force generation and overstretch of sarcomeres
. Diseases: cause inflammation

98
Q

Muscle fiber necrosis

A

. Occurs with damage to sarcolemma
. Excessive amounts of Ca enter into muscle from interstitial fluid
. Ca ions activate proteases that start to digest structural proteins
. Accompanied by release of growth factors and cytokines that stimulate immune system
. Significant swelling and edema
. WBCs enter necrotic area, continue the degradation of damaged structures and remove debris

99
Q

Muscle regeneration

A

. Initial step: satellite cells active
. Move to necrotic region and differentiate into myoblasts
. Myoblasts differentiate into myotubes
. Leads to regeneration and repair of damaged tissue through muscle protein synthesis

100
Q

Muscle injury during exercise

A

. Most injuries from eccentric contraction ( can occur in overstretched while unstimulated m.)
. Site of injury often at myotendinous junction
. Mechanical disruption of sarcolemma or in sarcomeres, assoc. w/ rise in Ca
. Lack of training and fatigue are most common predisposing factors

101
Q

Delayed onset muscle soreness (DOMS)

A

. Significant muscle soreness that peaks 24-48 hours after exercise
. Degree of discomfort depends on intensity and duration of exercise
. Experienced after unaccustomed exercise
. Most commonly associated w/ eccentric contractions
. Affects fast-twitch fibers more

102
Q

Observed changes in muscle during injury

A

. Osmotic pressure changes causing swelling
. Damage to sarcolemma
. Efflux from muscle of enzymes (esp creatine kinase) and myoglobin
. Altered ER function w/ poor control of cytosolic Ca concentration

103
Q

Cause of delayed soreness

A

. From acute inflammation and cellular swelling

. Processes activated by rise in cytosolic Ca

Physio (62 decks)

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