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IMS- Strand 10 > Neuromuscular transmission > Flashcards

Neuromuscular transmission Flashcards

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1
Q

What are the 2 types of synapses

A

Electrical synapses
Chemical synapses

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2
Q

What is an electrical synapse?

A

direct passage of current via ions flowing through gap junction between 2 neurones

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3
Q

What is a chemical synapse?

A

release of vesicles containing chemical transmitter which has an effect on receptors on a target cell

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4
Q

What is the connection on an electrical synapse between?

A

Direct physical connection between pre & post synaptic neurone
Connection takes form of a channel called a gap junction

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5
Q

What are 3 key functions of an electrical synapse?

A
  • Transmit signals more rapidly than chemical synapses do
  • Transmission can be bidirectional (can flow either direction depending on which cell receives the AP)
  • Enable the synchronized activity of groups of cells
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6
Q

What do gap junctions consist of?

A
  • hexameric complexes formed by the coming together of subunits called connexons, present in pre & post.
  • Pores of channels connect to one another creating electrical continuity between the two cells
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7
Q

What are chemical synapses?

A

-Connections between 2 neurons or between neuron & non neuronal cell
- One neuron releases neurotransmitter into the synapse adjacent to another cell
- Neurotransmitters bind to receptors on post cell and depending on nature of neurotransmitter can excite or inhibit PSC

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8
Q

How are neurotransmitters cleared from the synapse?

A
  • Enzyme degredation
  • Reuptake by specific transporters either on pre synaptic cell or on adjacent glial cell
  • Diffuse out of the synapse
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9
Q

What two types of post synaptic receptors can neurotransmitter bind to?

A

Ionotropic
Metabotropic

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10
Q

What are ionotropic receptors?

A

Group of transmembrane ion channels that open or close in response to the binding of the neurotransmitter
Fast acting= cause immediate change in membrane potential
e.g. nAChR

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11
Q

What are Metabotropic receptors?

A

Require G proteins and second messengers to indirectly modulate ionic activity in neurons
-generally slower more persistent response
e.g. nAChR

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12
Q

What is a neurotransmitter?

A

A substance that is released at a synapse by one neurone that affects another cell, either neuron or effector organ, in a specific manner

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13
Q

How are neurotransmitters classified?

A

either structure or function

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14
Q

What are excitatory neurotransmitters?

A

Increase electrical excitability at the post synaptic membrane to facilitate transmission of an action potential e.g. glutamate, acetylcholine

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15
Q

What are inhibitory neurotransmitters

A

reduce electrical excitability at the post synaptic membrane to prevent propagation of an action potential

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16
Q

What is a neuromodulator?

A

alter the strength of transmission between neurons by affecting the amount of neurotransmitter produced and released e.g.g endorphin

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17
Q

What is Glutamate?

A

one of the main excitatory neurotransmitters

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18
Q

What is GABA?

A

one of the main inhibitory neurotransmitters

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19
Q

What is the function of acetylcholine (ACh)?

A

Main parasympathetic neurotransmitter, involved in NMJ, learning, memory

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20
Q

What is the drug effects and pathology of acetylcholine?

A

Botox causes paralysis by blocking ACh release

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21
Q

What is the function of Noradrenaline?

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A

Used by the sympathetic nervous system, alertness, mood

22
Q

What are the drug effects and pathology of noradrenaline?

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A

Beta adrenergic receptor blockers (B-blockers) used to treat several cardiovascular pathologies including hypertension and heart failure

23
Q

What are the drug effects and pathology of GABA?

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A

Anti- anxiety drugs bind to GABA receptors supressing overactive brain areas linked to worry

24
Q

What are the drug effects and pathology of Glutamate?

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A

High levels associated with schizophrenia

25
What is the function of Serotonin?
Influences sleep, appetite, learning/ memory and mood
26
What are the drug effects and pathology of serotonin?
Serotonin- selective uptake inhibitiors are used to treat depression
27
What is the function of dopamine?
Pleasure neurotransmitter, influences learning/ memory, motivation/ behaviour, mood and movement
28
What are the drug effects and pathology of dopamine?
Drugs that increase dopamine are used in parkinson's
29
What are components of the motor unit?
- single motor neurone and all the skeletal muscle fibres innervated by that neurone - motor unit because when the motor neurone fires and AP it causes all muscle fibres that it innervates to contract within the unit at the same time - Size of motor unit depends on function of the muscle
30
How do motor units differ in different parts of the body?
- Thigh muscles= 1000s of muscle fibres in each unit - Smaller muscles have few muscle fibre in each motor unit= fine precision - The synapse between the motor neurone and the muscle cell is called a neuromuscular junction - A motor neurone innervating several muscle cells will have several axon terminals forming NMJs
31
What is a neuromuscular junction?
-Chemical synapse between a motor neurone and a muscle fibre -Site of transmission of AP from the nerve to the muscle -Unidirectional -Inherent time delay - Site for many diseases and action of many pharmacological drugs
32
What happens at a resting NMJ?
- Pre synaptic nerve terminal - Voltage gated Ca2+ channels - Motor end plate - Once every second, one synaptic vesicle fuses. with presynaptic terminal and release its content of ACh into synapse - ACh binds to the nAChR opening up Na+ channels - Entry of Na+ across the muscle membrane produce a small depolarisation called a MEPP
33
What are the 3 steps of an activated NMJ?
1- Arrival of AP causes depolarisation of axon terminal, voltage gated Ca2+ channels open 2- Ca2+ enters causing fusion of vesicles with presynaptic terminal and release of ACh 3- Several quants of ACh release into the synapse where they activate numerous nAChR resulting in the opening of Na+ channels and depolarisation of the muscle membrane. Each quantum can generate an MEPP in the muscle membrane, several quanta will lead to an EPP forming. If the EPP can depolarise the muscle membrane to threshold it triggers an AP
34
From MEPP to EPP to AP
- 1 vesicle contains ACh molecules~5000 molecules - Depolarisation produced by single quantum of ACh= MEPP~0.4mV - At rest= random occurrence - Following an AP- several quanta released - Resulting MEPPs are additive---> becoming end plate potentials (EPPS) - When EPPs cause the membrane to reach threshold voltage gated ion channels in the PSM open---> influx of Na+---> AP---> muscle contraction
35
What are EPPs?
end plate potentials
36
Excitation contraction coupling
- Links excitation of muscles by the nervous system to their mechanical contraction - EPP triggers AP in the muscle membrane - AP is propagated along the muscle membrane and wave of depolarisation passes down T-tubules - Within the T tubules the depolarisation is sensed by DHP receptors - Once activated, DHP receptors stimulate the opening of Ryanodine receptors (RyR) on the sarcoplasmic reticulum releasing Ca2+ into the cytoplasm of the muscle - Ca2+ used for muscle contraction - NMJ at centre of muscle fibre so AP is propagated towards both ends of the fibre allowing near simultaneous activation and contraction of the fibre
37
6 steps in events occuring at the synapse
1. ACh binds only briefly to nAChR on the post cell 2- Following dissociation from the receptor, the ACh is rapidly hydrolysed by enzyme acetylcholineesterase (AChE) 3- ACh hydrolyses to acetate+ choline 4- Choline recycled back into the presynaptic terminals (via transporters) to make more ACh 5- Acetate quickly diffuses into the surrounding medium 6- Some ACh will just diffuse out of the synaptic cleft
38
Structure of the nicotinic acetylcholine receptor (nAChR)
- The nAChR is an ACh- gated Na+ channel - Made up of 5 polypeptide subunits- two subunits and one of each B, delta, gamma - 2 ACh molecules required to stimulate the receptor the binding surface of the receptor= primarily on the a subunits, near the outer surface of the molecule - ACh binding to the receptor causes Na+ influx= membrane depolarisation - nAChR at autonomic ganglia & in brain have different subunit composition
39
How do drugs produce muscle paralysis?
- By affecting ACh receptors - Used during surgery to produce relaxation of skeletal muscle
40
What do muscle relaxants require?
the patient to be artificially ventilated
41
What does the toxin produced by clostridium botulinum do?
-prevents the exocytosis of ACh from synaptic vesicles - No ACh is released and the muscle does not contract - Toxin= botox
42
What do clinical injections of botox do?
Help patients with strabismus (cross eyes) Blepharospasm (eyelid spasms) cerebral palsy by helping to relax muscles with effects lasting 2-6 months
43
What is Myasthenia gravis?
Autoimmune response Caused by autoantibodies that competitively inhibit the nAChR on the motor end plate NMJ less responsive to ACh= muscle weakness
44
What are the symptoms of myasthenia gravis?
Muscle weakness that increases during periods of activity and improves after rest Greater than 50% present with eye- related issues as their initial symptom -ptosis= drooping of the eyelids - diplopia= double vision
45
15% of patients (myasthenia gravis)- symptoms involving face & throat muscles
- altered speech - difficulty swallowing, chewing - loss of facial expression The disease can also hit the limbs, both arms and legs, affecting their effective functional movement 20-35% of patients with thymoma also have myasthenia gravis
46
Pathophysiology at the NMJ (myasthenia gravis)
- Antibodies against the ACh receptor block receptors on the PSM, also get accelerated degradation of nACh receptor - Reduction of nACh receptors at the motor endplate and flattening of the postsynaptic folds reduce the EPP even though normal amount of ACh is being released - Reduced neuromuscular transmission causes reduced AP production on the motor end plate and muscle weakness
47
Treatment of myasthenia gravis
- Long term acting anti- cholinesterases- prevent breakdown of ACh- more ACh is available in the synapse to compete with the antibodies for the nAChR - Immunosuppressives- steroids - Surgical thymectomy= if appropriate
48
What is lamber eaton myasthenic syndrome?
- autoimmune disease - antibodies are formed against the voltage gated Ca2+ channels on the pre- synaptic nerve terminal at the NMJ= prevent ACh release - Condition often associated with small cell lung cancer
49
Symptoms of lamber eaton syndome
- weakness in muscle limbs - Fatigue - Autonomic dysfunction - Symptoms almost always precede detection of cancer- patients rarely complain of lung issues
50
Pathophysiology at the NMJ in Lamber eaton syndrome
- Antibodies disrupt the function of Ca2+ channels on the presynaptic neurone- block Ca2+ influx - Ca2+ entry during depolarisation is important for release of ACh into the synapse - Reduced Ca2+ influx--> reduces ACh release from presynaptic membrane---> reduced muscle activation---> muscle weakness
51
Treatment of Lamber eaton syndrome
- If underlying melignancy= treat to resolve the symptoms - Use immunosuppressants
52
What do K+ channel blockers do in treatment of lamber eaton syndrome
E.G. amifampridine (3,4 DAP) - blocks voltage gated K+ channels on pre synaptic nerve terminals - this delays the repolarisation of the membrane - so effectively prolongs depolarisation of presynaptic membrane - enhances Ca2+ entry into the terminal and so facilitates release of ACh - improves neuromuscular transmission

IMS- Strand 10 (3 decks)

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