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cells > muscle NMJ and choline > Flashcards

muscle NMJ and choline Flashcards

1
Q

distance and transmission time of NMJ

A

50nm gap between presynaptic terminal and post synaptic density
Delay of >500us between terminal release and muscle contraction

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2
Q

how does curare affect the NMJ

A

curare acts as a competitive inhibitor for ACh at the post synaptic terminal

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3
Q

how does alpha -bungarotoxin affect the NMJ

A

Alpha -bungarotoxin is known to bind competitively and in a relatively irreversible manner to the nicotinic acetylcholine receptor found at the neuromuscular junction, causing paralysis, respiratory failure, and death in the victim.

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4
Q

structure and function of nAChR

A

Pentamers of two alpha subunits with a beta theta and delta subunit
Each has two Ach binding sights on interface of Alpha and other subunits
Opening of channels increases membrane permibility for Na+and K+

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5
Q

where are nAChRs and voltage gated Na+ channels located on the post synaptic membrane?

A

nAChRs are localized in post synaptic density opposing presynaptic membrane
Voltage gated sodium channels are located in folds of the neuromuscular junction.

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6
Q

comment on the end plate potential compared with an action potential in a myocyte

A

End plate potential smaller than action potential but fires in similar structure

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7
Q

how can vesicles be imaged at the synapse

A

Because of active loading of synapes vesicles are verry acidic, and hence ph imaging can be used to monitor vesicles at a synapse

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8
Q

describe life cycle of a synaptic vesicle

A

Adapter protein bind to clathrin causing blebbing of the membrane
Dynamin acts as molecular scissors separating vesicle from membrane
> bind with endosome
> active acid loading then loading with neurotransmitter
Synapsin holds full vesicles in non membranous fluid density region
Synaptotagmin Binds with snare proteins and holds vesicle by membrane
Ca2+ release triggers fusing with the membrane

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9
Q

name and explain the function of the vesicular and membranous snare proteins

A

vesicular:
synaptobrevin- binds with SNAP-25 and syntaxin to hold the vesicle in place for release
synaptotagmin- is basis of Ca2+ sensing mechanism changes conformation to fuse with the membrane in presence of Ca2+
membranous:
SNAP-25 and syntaxin both function to hold the vesicles ready for docking

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10
Q

state the location and function of acetyl choline esterase

A

The basal lamina is very rich in AChE acetylcholinesterase which breaks down ACh rapidly in the neuromuscular junction. Ach is broken down into choline and acetic acid

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11
Q

how does the NMJ achieve high fidelity

A

Probability of any docked vesicle
being released <0.02
BUT
The entire frog NMJ has a total of 14,000–28,000 docked vesicles
350 vesicles released after every action potential
-> reliable suprathreshold response

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12
Q

how does botulinum toxin work

A

it is up taken in vesicles then cleaves snare proteins in the presynaptic terminal preventing neurotransmitter release

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13
Q

what is neuromyotonia

A

Autoimmune neuromyotonia is typically caused by antibodies that bind to potassium channels on the motor nerve resulting in continuous/hyper-excitability. Onset is typically seen between the ages of 15–60, with most experiencing symptoms before the age of 40.

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14
Q

what is myasthenia gravis

A

Myasthenia gravis is an autoimmune disease associated with antibodies directed to the postsynaptic acetylcholine receptor. These antibodies reduce the number of receptors. Autoantibodies against AChR and other muscle antigens can be used for the diagnosis of myasthenia gravis and related disorders.

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15
Q

what is lambert-eaton myathenic syndrome?

A

Lambert Eaton Myasthenic Syndrome (LEMS) is an autoimmune disorder characterised by proximal muscle weakness and autonomic symptoms. Approximately 60% of cases are paraneoplastic. Antibodies to presynaptic voltage gated calcium channels of the P/Q–type are detected in 92% of LEMS patients.

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16
Q

define sarcolema

A

The sarcolemma is the plasma membrane of the muscle cell

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17
Q

what is a sarcomere

A

the contractile unit of muscle cells

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18
Q

what is the z line and what purpose does it serve

A

Main function to bind sarcomeres together

Protine dense region many other functions

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19
Q

what is the M line

A

the m line binds heavy myosin chains together it also contains creatine kinase

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20
Q

what is the A band

A

consists of the darker area of overlapped myosin and actin with the M line at the center

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21
Q

what is the I band

A

the I band consists of the exposed actin centered around the very dark line of the Z band

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22
Q

describe structure of a triad

A

two loops of the SR coupled by proteins spanning the 35nm gap to a central t-tubule

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23
Q

describe how depolarization of the T-tubule causes Ca2+ release from the SR

A

1) Plasma depolarisation opens Ltype Ca2+ channels
2) Mechanical coupeling with the L- type calsium channel(LTCC) and Ryanodine receptor
3) Ca2+ exits via RyR activates tryponin C and triggers contraction
- Ca2+ entering via LTCC can also activate the RyR to open but this pathway (CICR) is not essential.

24
Q

what is a fascicle

A

a fasicle is a bundle of muscle fibers

25
Q

how does Ca2+ enable contraction

A

Ca2+ ions bind to tropnin Cor calmodulin in smooth muscle causing the troponin complex to shift
this causes a confrontational change in the tropomyosin moving it deeper into the actin groove uncovering the myosin binding sites thus enabling myosin binding and contraction

26
Q

in what 3 ways is contraction terminated

A

Major method is H+/Ca2+ ATPase co transporter into sarcolema.
2 minor mechanisms, Ca pump PMCA or Na-Ca exchanger, both move calcium to extra cellular space.

27
Q

explain the cross bridge cycle

A

ATP binds to to the myosin head causing it to un-couple with the Actin chain
The ATP is then hydrolyzed causing the myosin head to straighten such that its inline with a further point on the actin chain.
here a cross-bridge then forms
Release of the Phosphorous from the breakdown of ATP causes the ‘power stroke’ as the myosin head snaps back dragging the myosin along the actin chain
here the ADP is then released and the cycle begins a new

28
Q

explain what the IR stands for and how it relates to muscle strength

A

innervation ratio is the number of muscle cells that a single motor neuron innovates. Generally increase in innervation is correlated to muscle strength.

29
Q

explain the function and location of gap junctions in myocardium tissue

A

Between myocytes at intercalated disks
Allow ion movement between
6 connexin sub-units in conexome 2 connect form junction
Ca2+ one of the substances that regulate the aperture size of gap junctions/ opening. it deceases aperture size

30
Q

what is sterling’s law of the heart

A

As the more full the cardiac chambers the more stretch in the myocytes which confers greater contraction force of contraction due to the operating range of cardiac sarcomeres

31
Q 
explain the ionic vents that create the following phases in cardiac ventricular muscle
Phase 0: Fast upstroke. 
Phase 1: rapid repolarization.
Phase 2: plateau.
Phase 3: repolarization .
Phase 4; electrical diastolic phase.
A

Phase 0: Fast upstroke. Due to both ICa and INa (blocked by TTX).
Phase 1: rapid repolarization. Almost total inactivation of INa or ICa
Phase 2: plateau. Is prominent in VM. Continued entry of Ca2+ or Na+ ions through their major channels and on a minor membrane current due to the Na-Ca exchanger NCX1.
Phase 3: repolarization . It depends on IK
Phase 4; electrical diastolic phase. Vm during phase 4 is termed the diastolic potential.

32
Q

how does TTX (tetrodotoxin) affect nerve cells

A

It inhibits the firing of action potentials in neurons by binding to the voltage-gated sodium channels in nerve cell membranes and blocking the passage of sodium ions

33
Q

explain the phases and ionic events in a sinoatrial node potential

A

Phase 0: Slow upstroke, due only to ICa
Phase 3: repolarization . It depends on IK
Phase 4; electrical diastolic phase. In SA and AV nodal cells, changes in IK , ICa, and I f produce pacemaker activity (pacemaker potential or pacemaker current) during phase 4.

34
Q

how does adrenaline act on the heart muscle

A

through Gs coupled receptors that lead to phosphorylation of the L-type Ca2+ channels incresing the plateau phase
Phosphorylation of phospholamban (PLB), boosts Ca2+
re-uptake in SR

35
Q

how does adrenaline act on the san

A
  • Phosphorylation of LTCC (ICa-L), accelerates pacemaker potential decay
  • Phosphorylation of delayed rectifier K+ channel (IKV), increase in the outward current IKv contributes to the shortening of the action potential as well as pacemaker potential decay
36
Q

compare the effects of acetylcholine on the heart muscle wit adrenaline

A

much the opposite slows HR contractile force ect as coupled to Gi proteins instead

37
Q

Common features of smooth muscle cells

A

Spindle shaped cells 4-8µm diameter, 80-200 µm length, much smaller than striated muscle •
No striations: myofilaments not arranged as sarcomeres •
No T-tubules •
Sarcoplasmic reticulum present, but variable organization
Innervated by autonomic nerves
Organised into functional bundles

38
Q

Classification of smooth muscle:

A

Myogenic- contracts spontaneously e.g. the iris

Neurogenic- must be activated by nerves e.g. smooth muscles of arteries

39
Q

how is Ca2+ released into smooth muscle

A

ligand gated ion channels
CaV channels
Gq coupled receptors release out of SR

40
Q

How does calcium generate contraction in smooth muscle

A

Ca2+ binding protein, calmodulin (CaM) as Smooth muscle lacks troponin C
Caldesmon and calponin both calmodulin binding thin-filament proteins, inhibits myosin ATP’ase.
Inhibition removed by Ca2+-CaM
Slow actin-myosin dissociation, ‘latch-state’ conserves energy
Contraction also follows an increases in calcium sensitivity of contractile proteins

41
Q

3 Chemical classes of VGCC(voltage gated Ca2+ channels) Blocker

A

Dihydropyridines, e.g. nifedipine, amlodipine
Phenylalkylamines e.g verapamil
Benzothiazepines e.g. diltiazem All bind to the α1 subunit of L-type VGCCs, but at distinct sites Block calcium entry into smooth muscle cells

42
Q

how does doxazosin function

A

a1 adrenoceptor antagonists (doxazosin) blocks noradrenaline action from sympathetic nerves

43
Q

what effect does cGMP have on smooth muscle cells

A

decreases Ca2+ levels relaxing the cells

44
Q

ACh is an ester of what two chemicals

A

acetic acid and choline

45
Q

where is ACh found?

A 
At al autonomic ganglions (n&m)
Many autonomously innervated organs(n&m)
At NMJ(n)
46
Q

describe the life cycle of acetylcholine

A

choline + Acetyle CoA(from mitchondria)—choline acetyltransferase—-> ACh + CoA
loaded into vesicles by H+ anti-porters and released into cleft where its broken down by AChE (acetylcholinesterase )
into Choline and acetate.
choline is transported back into the cell and used to produce more ACh

47
Q

as nerves cannot produce enough choline where else is it acquired from?

A

Nerves cannot make enough choline so must be taken up from blood gained from diet and liver.

48
Q

mAChRs are found:

A

organs innervated by the parasympathetic division of the autonomic nervous system
autonomic ganglia,
and in the CNS
In the cns Muscarinic receptors are located pre and post synaptically
M1-5

49
Q

describe in detail nAChR receptor opening with reference to positive cooperativity

A

When inactive the 2nd membranous loop of each subunit has a kinked alpha helical structure that blocks pore conductance. ACh binding to the of the extracellular N terminus domains increases affinity of the second binding site for ACh this phenomenon is called positive cooperativity. Agonist binding causes a conformational alpha subunit twist that unkinks the alpha helical pore regions allowing ion conductance. The flow of Na+ and K+(equal permeability) down their electrochemical gradient causes an EPP (excitatory postsynaptic potential) in skeletal muscle and neurons.

50
Q

Name a mAChR antagonist

A

atropine

51
Q

name two toxins affecting ACh release

A

Alpha latrotoxin- massive release of vesicles causing depletion
Botulinum toxin breaks down snare proteins no ACh release

52
Q

snake venom’s can be useful in identifying receptors give an example

A

Snake venom useful in identifying receptor e.g. nAChR bound very tight by alpha cobratoxin

53
Q

Main effects of Muscarinic antagonists are:

A
  • Inhibition of secretions
  • Tachycardia
  • Pupillary dilation
  • Relaxation of smooth muscle (Bladder, gut, etc.)
54
Q

why must competitive antagonists for ACh be verry high affinity or high concentrations to be effective

A

80% of ACh receptors must be blocked to prevent any stimulus passing threshold
vecuronium and atracurium used clinically

55
Q

Acetylcholinesterases can also be used to decrese volontary movement name two such drugs

A

neostigmine and europhonium

cells (5 decks)

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