Module 3 Section 2.2 Flashcards

1
Q

Describe how the somatic nervous system is different from the autonomic nervous system.

A

Unlike the ANS, there is no inhibition of skeletal muscle contraction (only excitation). Thusm relaxation of skeletal muscle occurs by decreasing the excitability of motor neurons.

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2
Q

Outline the processes that occur b/w the excitation of a skeletal muscle.

A

.

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3
Q

Describe how black widow venom, botulinum toxin, and curare can lead to death.

A

Black widow venom

  • Causes an explosive release of ACh from all cholinergic sites. This overwhelms the ability of acetylcholinesterase to rapidly inactivate it and the result = prolonged depolarization.
  • During this, the voltage-gated Na channels are in their inactive state and can’t be stimulated.
  • If this happens at the diaphragm, contraction couldn’t be initiated and respiratory failure would occur.

Botulinum toxin

  • The toxin is released from the bacteria (Clostridium botulinum), which is a form of food poisoning.
  • Its action is the opposite of widow venom. It blocks the release of ACh from the terminal button. Subsequently, the skeletal muscle can’t be excited and paralysis occurs.
  • Less than 0.0001mg can kill an adult (by respiratory failure).

Curare

  • It’s a plant extract originating from Central and South American that has been used to create poison arrow heads.
  • Action occurs at the motor end plate where it binds to the same receptor as ACh. However, when it binds to the receptor, it does not cause an end plate potential. In other words, by binding the receptor, it is preventing ACh from binding to them.
  • Result = skeletal muscle is not excited, thus, causing muscle weakness and paralysis.
  • Death is by respiratory failure due to paralysis of the diaphragm.
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4
Q

What does stimulation of the somatic nervous system result in?

A

Stimulation = contraction and the release of ACh

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5
Q

What is the SNS comrised of?

A

The somatic nervous system is comprised of axons that innervates skeletal muscle under voluntary control.

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6
Q

Where are the cell bodies located in the SNS?

A

The cell bodies for all motor neurons (except the head) are located in the ventral horn of the spinal cord and their axons terminate directly on their effector, or target muscles.

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7
Q

Where do the upper motor neurons receive their info from?

A

The cortex, basal nuclei, cerebellum and brainstem.

They’re also receiving sensory input for the reflex pathways directly.

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8
Q

True or false: the motor neurons accept this collection of both excitatory (EPSPs) and inhibitory (IPSPs) signals to ultimately decide whether or not to generate action potentials and contract the muscles through lower motor neurons.

A

True

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9
Q

What is the difference between upper and lower motor neurons?

A

Upper motor neurons

  • Originate either in the motor region of the cerebral cortex or in the brain stem
  • Carries info fown to the lower motor neurons
  • They descend in the spinal cord to the level of the appropriate spinal nerve route

Lower motor neuron
- Located in either the anterior grey column, anterior nerve roots or the cranial nerve nuclei of the brainstem and cranial nerves w/ motor functions

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10
Q

What is the neuromuscular junction? Describe the structure.

A

The neuromuscular junction is where the neurotransmitter from the neuron stimulates the muscle fibre.

The terminal end of a motor neuron (terminal button) is a knob-like structure that fits into a shallow depression in the muscle fibre. There is a small cleft b/w the 2 structures.

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11
Q

Describe the mechanism of neurotransmitter release from a neuromuscular junction. (IMPORTANT)

A

1) An action potential in a motor neuron is propagated to the axon terminal (terminal button).
2) When an action potential reaches the terminal button, voltage-gates Ca channels open allowing Ca to enter the terminal button. This increase in Ca triggers the exocytotic release of vesicles containing ACh into the cleft.
3) The released ACh binds to nicotinic receptors on the motor end plate (region of the cleft below the terminal button) and opening cation channels. There’s a net influx of positive charge so the membrane potential depolarizes. This is the end-plate potential. End-plate potentials are graded and will increase in magnitude if more ACh is released and binds at the motor end plate.
4) Initiation of an action potential. When the end-plate potential depolarizes the motor end plate sufficiently, it influences the muscle membrane surrounding the motor end plate and voltage-gated Na channels begin to open. When sufficient Na channels open, the muscle fibre reaches threshold and the wave of excitation radiated out from the motor end plate causing the muscle to contract.
5) Every time a motor neuron is stimulated, it relseases ACh which then needs to be removed from the cleft or else the motor end plate and the muscle fibre would be in a constant state of excitation. This is accomplished by an enzyme called acetylcholinesterase, which inactivates ACh. This is a very quick process with all released ACh being inactivated within just a few milliseconds. This terminates the contraction signal.

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12
Q

If the following arrows were neurons in the body, what would be their corresponding titles: parasympathetic, sympathetic and motor neuron.

  • ————–>
  • ->0———->
  • ——>0—–>
A
  • ————–> motor neuron
  • ->0———-> sympathetic
  • ——>0—–> parasympathetic
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13
Q
Fill in the blank with the neurotransmitter (Epi Ach, or ACh) to match the corresponding synapse.
---------------> _
   _
-->0----------> _ and _ 
         _
------->0-----> _
A
---------------> ACh
  ACh
-->0----------> NE and Epi 
         ACh
------->0-----> ACh
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