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Tamsin - Physiology > Physiology of nerve and muscle cells > Flashcards

Physiology of nerve and muscle cells Flashcards

1
Q

What are the 3 types of muscle

A
  1. Skeletal muscle
  2. Cardiac musce
  3. Smooth muscle
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2
Q

What is resting membrane potential in nerves?

A

-70mV

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3
Q

What type of channels maintain the membrane potential?

A

K+ channels - K+ channel at rest is greater than Na+ channel

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4
Q

How do changes in Na and K affect the action potential

A

Changes in external K affect the resting membrane potential

  • If the extracellular concentration of K is increased (hyperkalaemia) the resting potential becomes closer to the threshold potential (less negative as less K flow out of cell) and the neuron becomes more excitable
  • If the extracellular level of K is reduced, the membrane potential is reduced and the membrane is hyperpolarised

Changes in external Na will affect the strength of the action potential

  • Decreasing the external Na+ reduces the size of the action potential but has little effect on the resting membrane potential (because permeability to Na+ is low
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5
Q

Describe the sequence of a nerve action potential

A

Depolarising stimulus > voltage gated Na+ channels open > Na+ enters the cell and there is a slow initial depolarisation (approx 15 mV) > reaches threshold potential > rate of depolarisation increases as more Na+ channels open > overshoots isopotential to +35 mV > Na+ influx slows and voltage gated K+ channels open > net movement of positive charge out of the cell > repolarisation > slow return of K+ channels to closed state > small but prolonged overshoot (afterhyperpolarisation)

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6
Q

What is the “all or none” principle

A

Once threshold intensity is reached, a full-fledged action potential is produced with constant amplitude and form regardless of the strength of the stimulus

If a weak stimulus is applied - it takes longer for the neuron to reach threshold level

If a strong stimulus is applied -there is short time to reach threshold

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7
Q

What is the absolute refractory period?

A

From moment firing level is reached until repolarisation is about 1/3 complete

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8
Q

What is relative refractory period?

A

From about 1/3 of repolarisation to the start of after depolarisation

Stronger than normal stimuli can cause excitation of the nerve during this period

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9
Q

What is saltatory conduction?

A

The way in which an electrical impulse skips from node to node down the length of an axon

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10
Q

What type of nerve fibres are most susceptible to local anaesthetic?

A

C

Local is important even if you CBA

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11
Q

What type of nerve fibres are most susceptible to hypoxia

A

B

Hypoxia needs oxygen BAC

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12
Q

Describe the conduction of an action potential

A
  • Nerve cell membrane is polarised at rest
    • +ve charges along the outside of the membrane
    • -ve charges along the inside of the membrane
  • During the action potential, polarity is abolished, + charges from the membrane ahead of and behind the action potential flow into the area of negativity represented by the action potential
  • By drawing off positive charges, this decreases the polarity of the membrane ahead of the action potential
  • This results in electrotonic depolarisation, which initiates a local response and when the firing level is reached a propogated reponse occurs.
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13
Q

What are type Aa nerve fibres?

A

Somatic motor and proprioception

Conduction velocity 70-120 m/s

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14
Q

What are type Ab nerve fibres?

A

Touch, pressure

Conduction velocity 30-70m/s

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15
Q

What are type Ag nerve fibres

A

Motor to muscle spindles (detect stretch in muscles)

Conduction velocity 15-30 m/s

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16
Q

What are type Ad nerve fibres?

A

Pain, temperature

Conduction velocity 12-30m/s

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17
Q

What are type B nerve fibres

A

Preganglionic autonomic

Conduction velocity 3-15 m/s

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18
Q

What are type C nerve fibres?

A

C-dorsal root - pain and temperature 0.5-2 m/s

C-sympathetic - post ganglionic sympathetic 0/7-2.3 m/s

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19
Q

What are the 3 differnt types of macroglia?

A
  1. Oligodendrocytes - emit multiple processes that form myelin on many neighbouring axons
  2. Schwann cells - form myelin on a single axon
  3. Astrocytes - found throughout the brain and are sibdivided into fibrous astrocytes (white matter) and protoplasmic astrocytes (gray matter). They produce substances that are tropic to neurons.
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20
Q

What are 4 key features of skeletal muscle?

A
  1. Has well developed cross-striations
  2. Contracts only as a consequence of nervous stimulation
  3. No functional connections between muscle fibres
  4. Under voluntary control
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21
Q

What are 3 key features of cardiac muscle?

A
  1. It has cross striations
  2. Does not require external innervation (has pacemaker cells)
  3. Is functionally syncytial
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22
Q

What are the key features of smooth muscle?

A
  1. Lacks cross-striations
  2. Can be further subdivided into 2 types
    1. Visceral - found in hollow viscera, contain pacemakers, functionally syncytial
    2. Multiunit - found in the eye, not spontaneously active
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23
Q

Describe the morphology of skeletal muscle

A
  • Each fibre is a single cell that is multinucleated, long, cylindrical and surrounded by the sarcolemma (cell membrane)
  • Muscle fibres are made up of myofibrils that are divisible in to individual filaments.
  • Myofilaments contain several proteins that make up the contractile machinery of the cell
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24
Q

What proteins are involved in the contractile mechanism of skeletal muscle?

A
  1. Myosin 2
  2. Actin
  3. Tropomyosin
  4. Troponin
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25
Q

Describe the structure of thick filaments

A
  • Made up of myosin 2
  • Has 2 heads (made up of light chains) and a long tail (made up of heavy chains)
  • The heads form cross-links to actin and contain an actin-binding site and a catalytic site that hydrolyses ATP
  • They are arranged symmetrically on either side of the centre of the centre sarcomere
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26
Q

Describe the structure of the thin-filaments

A
  • 2 chains of actin that form a long double helix
  • Tropomyosin forms long filaments located in the groove between the 2 chains of actin
  • Troponin molecules are located at intervals along the tropomyosin
    • Trop T - binds the other troponin components to tropomyosin
    • Trop I - inhibits the interaction of myosin with actin
    • Trop C - contains the binding sites for Ca2+ that initiates contraction
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27
Q

What is meant by the term sarcomere?

A

The area between two adjacent Z lines

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28
Q

Describe the lines and bands seen in a sarcomere

A
  • A band - Centre of the sarcomere, entire length of thick filament, appears darker due to overlap of actin and myosin filaments.
  • I band - The peripheries of the sarcomere which appear lighter as actin only is present
  • H zone - Light central region in the A band where only myosin is present
  • The light I band is divided by the dark Z line
  • The dark A band has the light H band at its centre
  • An M line is seen in the middle of the H band

(Way to remember: A band = All the myosin, I band - thin, thin filament only, H zone - thick, thick filament only, Z is at the end, M is in the middle)

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29
Q

What happens to the lengths of the different sarcomere bands when the muscle contracts?

A
  • The H zone reduces with contract (myosin filament not overlapping)
  • The A band never changes (myosin filament length)
  • The I band reduces with contraction (actin filament not overlapping)
  • Distance between Z lines and M lines also reduces with contraction
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30
Q

What is the function of actinin, titin and desmin?

A

Actinin - binds actin to the Z-lines

Titin - connects the Z lines to the M lines

Desmin - binds Z lines to plasma membrane

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31
Q

What is the sarcotubular system?

A

The sarcotubular system is made up of:

  1. The T system - Continuus with the sarcolemma, forms a grid perforated by individual muscle fibrils. Allows rapid transmission of the action potential from the cell to the plasma membrane
  2. The sarcoplasmic reticulum - Important store of Ca2+, forms an irregular curtain around each fibril. Has terminal cisterns in close contact with the T system.
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32
Q

What is the resting membrane potential of skeletal muscle?

A

-90mV

33
Q

What is meant by the term excitation-contraction coupling?

A

The process by which depolarisation of the muscle fibre initiates contraction

Action potential transmitted through T system > Calcium influx and release from sarcoplasmic reticulum > Calcium binds to trop C > confirmational change > myosin head cross bridging > myosin head rotates “power stroke” > ADP released > ATP binds, hydrolysis to ADP > myosin head re-cocked

34
Q

What are the steps involved in excitation and contraction?

A
  1. Discharge of motor neuron
  2. Release of Ach and binding to nicotinic Ach receptors
  3. Increased conductance of Na+ and K+ in the membrane
  4. Generation of end plate potential and transmission of action potential
  5. Spread of depolarisation along T tubules
  6. Release of Ca2+ from terminal cisterns of sarcoplasmic reticulum (via voltage gate dihydropyridine receptors) and diffusion to thick and thin filaments
  7. Ca2+ binds to troponin C which uncovers the myosin binding site on actin
  8. Formation of cross-linkages between actin and myosin and sliding of thin on thick filaments
35
Q

What are dihydropyridine receptors?

A
  • DHPRs are voltage gated Ca2+ channels in the T tubule membrane.
  • NOTE : In cardiac muscle, influx of Ca2+ via these channels triggers the release of Ca2+ stored in the sarcoplasmic reticulum by activating the Ryanodine receptor (RyR). In skeletal muscle, Ca2+ entry from the ECF by this route is not required, instead the DHPR triggers release of Ca2+ from the sarcoplasmic reticulum via phsyical interaction with the RyR.
36
Q

How does muscle relaxation come about?

A
  • Cytosolic Ca2+ concentration is reduced in the muscle cell by the SERCA (Sarcoplasmic or endoplasmic reticulum ATPase)
  • Once the Ca2+ concentration has been lowered sufficiently, ca2+ releases from troponin, chemical interaction between myosin and actin ceases and the muscle relaxes.
37
Q

Describe the sequence of events in the “power stroke” of skeletal muscle contraction

A
  1. At rest, myosin heads are bound to ADP and are said to be in a “cocked” position
  2. Ca2+ binds to the toponin-tropomyosin complex induces a confirmational change in the thin filament which allows for myosin heads to cross-bridge with thin filament actin
  3. The myosin heads rotate, move the attached actin and shorten the muscle fibre -“the power stroke”. ADP is released.
  4. ATP binds to a now exposed site and causes a detachment from the actin filament
  5. ATP is hydrolysed into ADP and Phosphate and this energy is used to re-cock the myosin head
38
Q

What is total tension

A

The sum of passive tension and active tension

  • Passive tension is the tension present due to intrinsic elastic nature of muscle - this will increase with muscle length until the muscle ruptures
  • Active tension - tension generated by the contraction process. At the resting length there is optimal alignment of actin and myosin and the length of the muscle is considered to be at its greatest mechanical advantage
39
Q

What are type 1 skeletal muscle fibres?

A
  • Slow, oxidative
  • Red
  • Small diameter
40
Q

What are type 2a skeletal muscle fibres?

A
  • Fast, oxidative, glycolytic (FOG)
  • Red
  • Large
41
Q

What are type 2b skeletal muscle fibres?

A
  • Fast, glycolytic (FG)
  • White
  • Large
42
Q

What is phosphorylcreatine?

A
  • Energy rich compound sitting in myocytes
  • Hydrolysed at the junction between myosin heads and actin, forming ATP from ADP and creatine.
43
Q

What are the energy sources of skeletal muscle

A
  • At rest and during light exercise - free fatty acids (FFA)
  • As intensity increases, use of carbohydrate becomes the predominant component
  • Glucose is converted to pyruvate, pyruvate enters the citric acid cycle and is metabolised to CO2 and H2O
  • If O2 supplies are insufficient the pyruvate formed does not enter the tricarboxylic acid cycle but is reduced to lactate - produces much smaller quanitites of ATP but does not require O2.
44
Q

What is oxygen debt in skeletal muscle?

A
  • When muscular exertion is great, aerobic resynthesis of ATP stores cannot keep pace with their utilisation.
  • Phosphorylcreatine is used to resynthesize ATP and some ATP is released by the anaerobic breakdown of glucose to lactate
  • After a period of exertion, extra O2 is consumed to remove the excess lactate, replenish the ATP and phosphorylcreatine stores and replace the small amounts of O2 that were released by myolgobin
  • Rigor occurs when ATP is completely depleted (eg in rigor mortis) resulting from abnormal and dixed binding of myosin heads to actin
45
Q

What is meant by the term motor unit?

A

A single motor nueron and the fibres it innervates

46
Q

What are the different types of motor unit?

A

S - Slow (usually low innervation ratio- small units)

FR - Fast, Resistant to fatigue

FF - Fast, fatiguable (usually high innervation ratio - large units)

Order of recruitment: S –> FR –> FF

47
Q

Compare the morphology of cardiac muscle to skeletal muscle

A
  • Striations are similar, Z lines present
  • Muscle fibres in caradiac muscle branch and interdigitate
  • Intercalated discs (strong union between fibres) creating cell to cell cohesion
  • Gap junctions - cell membranes of adjacent fibres fuse allowing cardiac muscle to function as a syncytium
  • The T system in cardiac muscle is located at the Z lines rather than the AI junction
48
Q

What is resting membrane potential in cardiac cells?

A

-90mV

Depolarisation lasts about 2ms

Plateau phase and repolarisation lasts 200ms or more

49
Q

Describe the action potential in a typical ventricular cardiomyocyte

A

Resting membrane potential > Phase 0 Initial rapid depolarisation due to opening of voltage gated Na+ channels > Phase 1 - initial rapid repolarisation due to closure of Na+ channels > Phase 2 - plateau phase due to slower but prolonged opening of voltage gated Ca2+ channels > Phase 3 -final repolarisation due to closure of Ca2+ channels and K+ efflux through various types of k+ channels > Phase 4 - resting membrane potential

The absolute refractory period lasts from phase 0 to 1/2 way through phase 3

50
Q

Describe how excitation-contraction coupling differs in skeletal and cardiac muscle

A

In cardiac muscle, it is the influx of Ca2+ through the voltage sensitive DHPR in the T tubule membrane which triggers Ca2+ induced Ca2+ release through the RyR at the sarcoplasmic reticulum.

In skeletal muscle the DHPR is activated, resulting in confirmational change which activates the RyR at the sarcoplasmic reticulum ( ie Ca2+ release from the SR is not dependant on Ca2+ influx through the DHPR)

51
Q

Describe the process of exctiation-contraction coupling in cardiac muscle

A
  1. Action potential arrives at the T tubule and depolarises the membrane
  2. Voltage gated DHPR (L-type) open to permit calcium entry into the cell during phase 2 of the action potential
  3. Calcium influx triggers a subsequent release of calcium that is stored in the SR through ryanodine receptors (RyR)
  4. Free calcium binds to trop C, inducing a confirmational change such that trop I exposes the myosin binding site on actin.
  5. Upon binding, ADP is released causing a confirmational change that moves the thin filament rleative to the thick filament comprising “the power stroke”
  6. ATP binds to the free site on myosin which leads to detachment of the myosin head the actin
  7. ATP is hydrolysed releasing phosphate, causing a “re-cocking” of the myosin head
52
Q

What is the correlation between muscle fibre length and tension in the heart ?

A
  • Initial fibre length is determined by diastolic filling in the heart
  • The pressure developed in the ventricle is proportional to the volume of the ventricle at the end of the filling phase (Starling law of the heart)
  • The developed tension increases as the diastolic volume increases until it reaches a maximum then tends to decrease
53
Q

Describe the role of cAMP in the positive inotropic effect of catecholamines in the heart

A
  • cAMP activates protein kinase A
  • This leads to phosphorylation of voltage gated calcium channels causing them to spend more time in the activated state
  • cAMP increases the active transport of Ca2+ into the sarcoplasmic reticulum via the SERCA which accelerates relaxation and consequently shortens systole - this helps permit adequate diastolic filling
54
Q

Under basal conditions where are the caloric needs of the heart supplied from?

A

60% fat

35% carbohydrate

5% ketones and amino acids

55
Q

Describe the morphology of smooth muscle compared to cardiac and skeletal muscle

A
  • Lacks cross striations
  • Actin and myosin2 are not arranged in regular arrays as in skeletal and cardiac muscle
  • Instead of Z lines there are dense bodies in the cytoplasm attached to the cell membrane which are bound by a-actinin to actin filaments
  • Smooth muscle contains tropomyosin but troponin is absent
  • Smooth muscle has a less extensive SR
  • Few mitochondria
56
Q

What are the 2 types of smooth muscle?

A

Unitary - visceral smooth muscle eg hollow viscus

  • Occurs in large sheets
  • Many low resistance gap junctions
  • Functions in syncytial fashion

Multiunit smooth muscle eg the iris

  • Indivudal units with few or no gap junctions
  • Many functional similarities to skeletal muscle but not under functional control
57
Q

What are the elctrophysiological properties of smooth muscle?

A
  • Instability of the membrane potential - no true “resting” value
  • Continuus irregular contractions - tonus
58
Q

Describe the molecular basis of contraction in smooth muscle

A
  • Ca2+ increase can be due to:
    • Influx through voltage gated or ligand gated channels in the plasma membrane
    • Release or mobilisation from intracellular stores through the RyR and the IP3R receptor
  • Lack of tropnin in smooth muscle prevents Ca2+ activation via troponin binding
  • Myosin in smooth muscle must be phosphorylated for the action of myosin ATPase
  • Ca2+ binds to calmodulin, the resulting complex activates calmodulin-dependant myosin light-chain kinase which catalyses the phosporylation of the myosin light chain on serine at position 19, increasing its ATPase activity
  • Myosin is dephosphorylated by myosin light-chain phosphatase-this does not necessarily lead to relaxation of the smooth muscle
59
Q

What is the sequence of events in contracitn and relaxation of visceral smooth muscle

A
  1. Binding of Ach to muscarinic receptors
  2. Influx of Ca2+ into the cell (mediated by PLC –> IP3 and Ca2+ channel opening)
  3. Activation of calmodulin depenant myosin light chain kinase
  4. Phosphorylation of myosin
  5. Increased myosin ATPase activity and binding of myosin to actin
  6. Contraction
  7. Dephosphorylation of myosin by myosin light chain phosphatase
  8. Relaxation or sustained contraction
60
Q

Why is unitary smooth muscle unique compated to other types of muscle

A

It contracts when stretched in absence of any extrinsic innervation

Stretch is followed by a decline in membrane potential (depolarisation), and increase in the frequency of spikes and a general increase in tone

61
Q

What is the effect of epinephrine or norepinephrine on intestinal smooth muscle?

A

Membrane potential becomes larger (more negative, hyperpolarised) and the spikes decrease in frequency –> relaxation

62
Q

What is the effect of acetylcholine on intestinal smooth muscle?

A

The membrane potential decreases (less negative or depolarisation), the spikes become more frequent. The muscle becomes more active –> contraction. Mediated by phospholipase C and IP3.

63
Q

What are the 2 most common types of synapse in the cerebral cortex?

A

Axo-dendritic

Axo-somatic

64
Q

What are the 3 types of vesicle found in the pre-synaptic button

A
  • Small clear vesicles (Ach, glutamate, GABA)
  • Small dense-cored vesicles (catecholamines)
  • Large dense-cored vesicles (neuropeptides)

The vesicles and the proteins contained within them are synthesized in the neuronal cell body and transported along the axon to the endings by fast axoplasmic transport

65
Q

What are neurexins?

A

Presynaptic cell adhesion molecules that bind to neuroligins on the membrane of postsynaptic neurons

66
Q

How wide is the synaptic cleft?

A

20-40nm

67
Q

What is responsible for synaptic delay?

A

The delay is the time it takes for the synaptic mediator to be released and act on the receptors on the membrane of the postsynaptic neuron.

The minmum time for transmission across one synapse is 0.5 ms

68
Q

What produces a slow EPSP/IPSP

A

Slow postsynaptic potentials have a latency of 100-500ms and last several seconds

Slow EPSPs are usually due to decreases in K+ conductance

Slow IPSPs are due to increases in K+ conductance

69
Q

What are excitatory postsynaptic potential (EPSPs) ?

A

A single stimulus applied to a sensory nerve does not lead to the formation of a propagated action potential

Instead the stimulation produces either a transient partial depolarisation or a transient hyperpolarisation

An EPSP is a transient parital depolarisation which increases the excitablity of the nueron to other stimuli

70
Q

Explain how a fast EPSP is produced

A
  • Excitatory neurotransmitter opens Na+ or Ca2+ channels in the postsynaptic membrane, producing an inward current.
  • This does not drain off enough positive charge to depolarise the whole membrane, rather a small EPSP is produced
  • The EPSP begins 0.5ms after the afferent impulse, reaches its peak 1-1.5ms later and then declines exponentially
71
Q

What is an IPSP?

A

Stimulation of some inputs produces hyperpolarising responses. During this potential the excitability of the neuron to other stimuli is decreased. This is a fast inhibitory post synaptic potential (IPSP)

A fast IPSP can be produced by a localised increase in Cl- transport causing net hyperpolarisation. Opening of K+ channels or closure of Na+ or Ca2+ channels can also cause an IPSP

Released neurotransmitter triggers the opening of Cl- channels > Cl- moves down its concerntration gradient > transfer of negative charge into cell > increasing membrane potential > decreased excitability

72
Q

Which portion of a motor neurone has the lowest threshold for the production of an action potential?

A

The initial segment - the portion of the axon at and just beyond the axon hillock. It is the first part of the neuron to fire and its dischrage is propagated in two directions: down the axon and back into the soma

73
Q

What are temporal summation and spatial summation?

A

Central neurons integrate a variety of synaptic inputs through temporal and spatial summation

Temporal summation

  • The time constant of the postsynaptic neuron affects the amplitude of the depolarisation caused by 2 consecutive EPSPs produced by a single presynaptic neuron
  • The time constant of a neuron determines the time course of the synaptic potential - the longer the time constant the greater the chance for 2 APs to summate to induce an AP

Spatial summation

  • The length constant of a postsynaptic cell affects the amplitude of two EPSPs produced by two pre-synaptic neurons
  • The length constant determines the degree to which a depolarising current is reduced as it spreads passively - a long length constant means the membrane depolarisation from 2 trigger points can spread to the trigger zone with minimal decrement .
74
Q

What is direct and indirect inhibition within the CNS?

A

Direct inhibition

  • Post synaptic inhibition during the course of an IPSP
  • Not a consequence of previous discharges of the postsynaptic neuron

Indirect inhibition

  • Inhibition due to the effects of previous neuron discharge
    • eg refractory period, afterhyperpolarisation
75
Q

What is post synaptic inhibition?

A

When an inhibiotry neurotransmitter such as glycine or GABA is released from a presynaptic nerve terminal onto the posysynaptic neuron to induce an IPSP in the postsynaptic neuron

76
Q

What is presynaptic inhibition

A
  • Mediated by neurons that end on excitatory endings-axoaxonal synapses
  • 3 mechanisms:
    • Activation of presynaptic receptors > increased Cl- conductance > decreases size of APs reaching the excitatory ending > reduced Ca2+ entry > reduced amount of excitatory neurotransmitter released
    • Opening of voltage-gated K+channels > K+ efflux > decreased Ca 2+ influx
    • Direct inhibition of transmitter release, indepenant of Ca2+ influx into the excitatory ending
  • The first neurotransmitter shown to produce presynaptic inhibiton was GABA
77
Q

What are the different types of GABA?

A

GABA A - Increases Cl- conductance

GABA B - Mediate presynaptic inhibition via a G protein that produces an increase in K+ conductance eg Baclofen - a GABA B agonist

78
Q

When is presynaptic facilitation produced

A

When the action potential is prolonged, the Ca2+ channels are open for a longer period

eg Serotonin - increased cAMP > Phosphrylation of K+channels > channels close > slows repolarisation > prolongs AP

79
Q

What are Renshaw cells ?

A

Inhibitory interneurons in the spinal cord that provide negative feedback to motor neurons

Tamsin - Physiology (4 decks)

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