Neuromuscular Transmission ppt 7 Flashcards

1
Q

What is an NMJ?

A

Neuromuscular junction , the axons of motor neurons innervate skeletal muscle fibers.
The neuron intercept at the motor end plate

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2
Q

What are key features of a peripheral synapse?

A
  • Only one motor neuron innervates a muscle fiber,
  • Only excitatory input (no inhibitory input) is received by each muscle fiber,
  • Only one neurotransmitter (Ach) activates the muscle fibers
  • One kind of receptor channel (nicotinic acetylcholine receptor channel)
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3
Q

What are the key features of a central synapse?

A
  • More complex than that at the nerve-muscle synapse.

- Inhibitory as well as excitatory inputs to a central neuron.

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4
Q

What is Myasthenia Gravis?

A

Is an autoimmune disease in which antibodies attack the Nicotinic Ach receptors.
Prevents the Muscle Contraction

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5
Q

What are the typical symptom of myasthenia graves?

A

muscle weakness that increases during periods of activity and improves after periods of rest

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6
Q

Myasthenia graves is usually associated with

A

underlying thymoma

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7
Q

What is a Tension test?

A

A test fo MG

Administration of edrophonium, a short acting AchE inhibitor, rapidly improves symptoms

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8
Q

What is abnormally elevated in patients with MG?

A
ACh antibodies. 
AntiMuSK antibody (30-40%)
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9
Q

What is the treatment for MG?

A

AChE inhibitors

Thymectomy

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10
Q

What is Lambert Eaton syndrome (LEMS)?

A

-Auto immune disease in which antibodies attack calcium channels in the PRESYNAPTIC terminal.

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11
Q

What are the typical symptoms of LEMS?

A
  • Weakness of proximal arms and legs
  • Affects the legs more than the arms.
  • Difficulties climbing stairs and rising from a sitting position
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12
Q

LEMS is usually associated with

A

small cell lung cancer?

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13
Q

As oppose to MG, LEMS usually improves with

A

Exercise

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14
Q

What is Botulism?

A

-Clostridium botulinumis a bacterium that produces dangerous toxins that block nerve functions and can lead to respiratory and muscular paralysis.

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15
Q

What is the mechanism of action for Botulinum toxin?

A

Botulinum toxin is a specific protease that cleaves SNARE proteins present in the vesicular and presynaptic cell membranes. These SNARE proteins are involved in exocytosis, preventing the release of neurons transmitters.

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16
Q

What is the time os incubation for botulinum toxin?

A

normal: 12-36 hour

can be 6hr- 10 days

17
Q

What is the presentation of a baby with infantile botulism?

A

Classic presentation for infantile botulism includes antecedent constipation with the ascending paralysis, ptosis, dilated or unreactive pupils, and weakness in the arms and legs.

18
Q

What causes infantile botulism?

A

Spores in Honey

Types A and B- BAby

19
Q

What is wound botulism?

A
  • Spores get into an open wound and are able to reproduce in
  • Two weeks to appear.
  • Associated with injecting black tar heroin.
20
Q

What is inhalation botulism?

A
  • Does not occur naturally, it is associated with accidental or intentional (e.g. bioterrorism)
  • The median lethal is three times greater than in foodborne cases.
21
Q

What is tetanus?

A
  • Clostridium bacteria that produce tetanus toxin.
  • 7 to 21 days.
  • Inhibitory spinal interneurons. Damage to which results in disinhibition of spinal motor neurons.
  • Hyperexcitation= tetanic contractions
22
Q

What is the MOA of tetanus toxin?

A

Protease that cleaves SNARE proteins, abolition of release of inhibitory neurotransmitter from spinal interneurons.

23
Q

What is a neurotransmitter?

A

Chemical substance that is synthesized in a neuron, released at a synapse to elicit a specific response.

24
Q

What is neruomodulator?

A

Chemical messenger released by a neuron that does not directly cause EPSPs or IPSPs but instead affects the strength of synaptic transmission.

25
Q

What are the major classes of neurons transmitters?

A
  • Small molecule
  • Neuropeptides
  • Gaseous
26
Q

What the are major Small molecule Nero transmitters?

A
  • Acetylcholine
  • Excitatory: glutamate and aspartate
  • Inhibitory: GABA and Glycine
27
Q

What are the major Neuropeptides?

A
  • Opioid peptides: b-endorphin, methionine-enkephalin, leucine-enkephalin, endomorphs, nociceptin.
  • Substance P
28
Q

How are presynaptic vesicles formed?

A
  • Vesicles are synthesized in the presynaptic cell body, shuttled by fast or slow axonal transport to the nerve terminal. Filled locally produced neurotransmitter.
  • Peptide transmitters are synthesized and prepackaged in vesicles within the cell body rather than in the nerve terminal.
29
Q

Where are neurotransmitters contained?

A
  • Small-molecule transmitters: clear-core vesicles.

- Serotonin and norepinephrine are exceptions: contained in dense-core vesicles

30
Q

What is transported via slow axonal transport?

A
  • The propeptide and enzyme-filled vesicles.
  • Soluble enzymes (e.g.,acetylcholinesterase, tyrosine hydroxylase )
  • Enzymes cleave the propeptide to produce a smaller peptide transmitter that remains in the large dense-core vesicles.

31
Q

What does the SNARE protein complex include?

A

Synaptobrevin, syntaxin, and SNAP-25.

32
Q

What are the steps of release from a synaptic membrane?

A
  1. Action potential arrives and opens Ca2+ channels.
  2. Ca2+ brings to protein called synaptotagmin
  3. Activates SNARE
  4. Vesicles fuse and empty contents
33
Q

Excitatory vs Inhibitory receptors

A
  • Excitatory receptors (NMDA) cause membrane depolarization, Increased firing rates
  • Inhibitory receptors (GABA) hyperpolarize the membrane and decrease spike frequency.
34
Q

Ionotropic vs Metabotropic

A
  • Ionotropic receptors usually consist of multimeric proteins and form the pore of the ion channel (aka. ligand-gated
) SHORT DURATION
  • Metabotropic Receptors flow of ions depends on one or more metabolic steps. (Gprotein)
35
Q

How is a signal terminated?

A
  • Signal degradation: acetylcholinesterase – breaks down ACh
  • Recycle: choline taken back up, reused to make new acetylcholine
  • Diffusion